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Reductionists would claim that athletic success comes down to the molecular level. I disagree. Though, of course, understanding the molecular pathways and how and why certain athletes excel in certain sports can and will increase our understanding of elite athleticism, reductionist accounts do not tell the full story. A reductionist (which I used to be, especially in regard to sports; see my article Racial Differences in Muscle Fiber Typing Cause Differences in Elite Sporting Competition) would claim that, as can be seen in my article, the cause for elite athletic success comes down to the molecular level. Now, that I no longer hold such reductionist views in this area does not mean that I deny that there are certain things that make an elite athlete. However, I was wrong to attempt to reduce a complex bio-system and attempt to pinpoint one variable as “the cause” of elite athletic success.
In the book The Genius of All of Us: New Insights into Genetics, Talent, and IQ, David Shenk dispatches with reductionist accounts of athletic success in the 5th chapter of the book. He writes:
2. GENES DON’T DIRECTLY CAUSE TRAITS; THEY ONLY INFLUENCE THE SYSTEM.
Consistent with other lessons of GxE [Genes x Environment], the surprising finding of the $3 billion Human Genome Project is that only in rare instances do specific gene variants directly cause specific traits or diseases. …
As the search for athletic genes continues, therefore, the overwhelming evidence suggests that researchers will instead locate genes prone to certain types of interactions: gene variant A in combination with gene variant B, provoked into expression by X amount of training + Y altitude + Z will to win + a hundred other life variables (coaching, injuries, etc.), will produce some specific result R. What this means, of course, What this means, of course, is that we need to dispense rhetorically with thick firewall between biology (nature) and training (nurture). The reality of GxE assures that each persons genes interacts with his climate, altitude, culture, meals, language, customs and spirituality—everything—to produce unique lifestyle trajectories. Genes play a critical role, but as dynamic instruments, not a fixed blueprint. A seven- or fourteen- or twenty-eight-year-old is not that way merely because of genetic instruction. (Shenk, 2010: 107) [Also read my article Explaining African Running Success Through a Systems View.]
This is looking at the whole entire system: genes, to training, to altitude, to will to win, to numerous other variables that are conducive to athletic success. You can’t pinpoint one variable in the entire system and say that that is the cause: each variable works together in concert to produce the athletic phenotype. One can invoke Noble’s (2012) argument that there is no privileged level of causation in the production of an athletic phenotype. There are just too many factors that go into the production of an elite athlete, and attempting to reduce it to one or a few factors and attempt to look for those factors in regard to elite athleticism is a fool’s errand. So we can say that there is no privileged level of causation in regard to the athletic phenotype.
In his paper Sport and common-sense racial science, Louis (2004: 41) writes:
The analysis and explanation of racial athleticism is therefore irreducible to
biological or socio-cultural determinants and requires a ‘biocultural approach’
(Malina, 1988; Burfoot, 1999; Entine, 2000) or must account for environmental
factors (Himes, 1988; Samson and Yerl`es, 1988).
Reducing anything, sports included, to environmental/socio-cultural determinants and biology doesn’t make sense; I agree with Louis that we need a ‘biocultural approach’, since biology and socio-cultural determinants are linked. This, of course, upends the nature vs. nurture debate; neither “nature” nor “nurture” has won, they causally depend on one another to produce the elite athletic phenotype.
Louis (2004) further writes:
In support of this biocultural approach, Entine (2001) argues that athleticism is
irreducible to biology because it results from the interaction between population-based genetic differences and culture that, in turn, critiques the Cartesian dualism
‘which sees environment and genes as polar-opposite forces’ (p. 305). This
critique draws on the centrality of complexity, plurality and fluidity to social
description and analysis that is significant within multicultural common sense. By
pointing to the biocultural interactivity of racial formation, Entine suggests that
race is irreducible to a single core determinant. This asserts its fundamental
complexity that must be understood as produced through the process of
articulation across social, cultural and biological categories.
Of course, race is irreducible to a single core determinant; but it is a genuine kind in biology, and so, we must understand the social, cultural, and biological causes and how they interact with each other to produce the athletic phenotype. We can look at athlete A and see that he’s black and then look at his somatotype and ascertain that the reason why athlete A is a good athlete is conducive to his biology. Indeed, it is. One needs a requisite morphology in order to succeed in a certain sport, though it is quite clearly not the only variable needed to produce the athletic phenotype.
One prevalent example here is the Kalenjin (see my article Why Do Jamaicans, Kenyans, and Ethiopians Dominate Running Competitions?). There is no core determinant of Kalenjin running success; even one study I cited in my article shows that Germans had a higher level of a physiological variable conducive to long-distance running success compared to the Kalenjin. This is irrelevant due to the systems view of athleticism. Low Kenyan BMI (the lowest in the world), combined with altitude training (they live in higher altitudes and presumably compete in lower altitudes), a meso-ecto somatotype, the will to train, and even running to and from where they have to go all combine to show how and why this small tribe of Kenyans excel so much in these types of long-distance running competitions.
Sure, we can say that what we know about anatomy and physiology that a certain parameter may be “better” or “worse” in the context of the sport in question, no one denies that. What is denied is the claim that athleticism reduces to biology, and it does not reduce to biology because biology, society, and culture all interact and the interaction itself is irreducible; it does not make sense to attempt to partition biology, society, and culture into percentage points in order to say that one variable has primacy over another. This is because each level of the system interacts with every other level. Genes, anatomy and physiology, the individual, the overarching society, cultural norms, peers, and a whole slew of other factors explain athletic success not only in the Kalenjin but in all athletes.
Broos et al (2016) showed that in those with the RR genotype, coupled with the right morphology and fast twitch muscle fibers, this would lead to more explosive contractions. Broos et al (2016) write:
In conclusion, this study shows that a-actinin-3 deficiency decreases the contraction velocity of isolated type IIa muscle fibers. The decreased cross-sectional area of type IIa and IIx fibers may explain the increased muscle volume in RR genotypes. Thus, our results suggest that, rather than fiber force, combined effects of morphological and contractile properties of individual fast muscle fibers attribute to the enhanced performance observed in RR genotypes during explosive contractions.
This shows the interaction between the genotype, morphology, fast twitch fibers (which blacks have more of; Caeser and Henry, 2015), and, of course, the grueling training these elite athletes go through. All of these factors interact. This further buttresses the argument that I am making that different levels of the system causally interact with each other to produce the athletic phenotype.
Pro-athletes also have “extraordinary skills for rapidly learning complex and neutral dynamic visual scenes” (Faubert, 2013). This is yet another part of the system, along with other physical variables, that an elite athlete needs to have. Indeed, as Lippi, Favalaro, and Guidi (2008) write:
An advantageous physical genotype is not enough to build a top-class athlete, a champion capable of breaking Olympic records, if endurance elite performances (maximal rate of oxygen uptake, economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) (Williams & Folland, 2008) are not supported by a strong mental background.
So now we have: (1) strong mental background; (2) genes; (3) morphology; (4) Vo2 max; (5) altitude; (6) will to win; (7) training; (8) coaching; (9) injuries; (10) peer/familial support; (11) fiber typing; (12) heart strength etc. There are of course myriad other variables that are conducive to athletic success but are irreducible since we need to look at it in the whole context of the system we are observing.
In conclusion, athleticism is irreducible to biology. Since athleticism is irreducible to biology, then to explain athleticism, we need to look at the whole entire system, from the individual all the way to the society that individual is in (and everything in between) to explain how and why athletic phenotypes develop. There is no logical reason to attempt to reduce athleticism to biology since all of these factors interact. Therefore, the systems view of athleticism is the way we should view the development of athletic phenotypes.
(i) Nature and Nurture interact.
(ii) Since nature and nurture interact, it makes no sense to attempt to reduce anything to one or the other.
(iii) Since it makes no sense to attempt to reduce anything to nature or nurture since nature and nurture interact, then we must dispense with the idea that reductionism can causally explain differences in athleticism between individuals.
That High-School Running Competition: Anatomic and Physiologic Differences Between Men and Women and the Possibility of Sports Segregation by Anatomy and Physiology
Recently there has rightly been, much written about a certain high-school running competition. The competition in question was a girl’s high-school in-door state competition in Connecticut. The first two spots went to two transgender athletes, as if that is a surprise to anyone who knows basic body mechanics and anatomy and physiology. What really irks me about this is that it is demoralizing to the women who train hard year-round, who eat right and have the right mindset to be able to compete in these competitions. Then men who “identify” as women just pretty much walk onto the track and blow away the competition. In this article, I will discuss anatomical and physiological differences between the sexes and how and why these competitions are segregated. Finally, I will discuss Roslyn Kerr’s thoughts on why it may be time to end sex segregation in sports, because she drives a very compelling argument—and this may end the current problems we have regarding these current controversies in high-school—and all—sports.
I have previously written on transgender athletes competing in weight-lifting and the IOC’s (International Olympic Committee’s) guidelines on testosterone levels and “acceptable limits” regarding “transitioning” athletes. The IOC writes:
The athlete must demonstrate that her total testosterone level in serum has been below 10 nmol/L for at least 12 months prior to her first competition (with the requirement for any longer period to be based on a confidential case-by-case evaluation, considering whether or not 12 months is a sufficient length of time to minimize any advantage in women’s competition).
The athlete’s total testosterone level in serum must remain below 10 nmol/L throughout the period of desired eligibility to compete in the female category.
Compliance with these conditions may be monitored by testing. In the event of non-compliance, the athlete’s eligibility for female competition will be suspended for 12 months.
This is very strange to me. Quoting myself:
10 nanomoles per liter of blood converts to about 288 ng/dl (nanograms per deciliter). Going with the lower end suggested by other members of the IOC, 3 nanomoles per deciliter of blood converts to 87 ng/dl. The range for women is 15 to 70 ng/dl. Now, the 10 nmol/l is, as you can see, way too high. However, 10 nmol/l converts to slightly higher than the lower end of the new testosterone guidelines for the average male in America and Europe (which I covered yesterday, the new levels being 264-916 ng/dl). As we can see, even 10 nmol/l is way too high and, in my opinion, will give an unfair advantage to these athletes
10 nanomoles per liter of blood converts to slightly higher than the lower end for males. How is that fair, in any capacity? Though it is worth noting that other members of the IOC have contested this, saying that 10 nmol/L is too high. In any case, this discussion is really about what should happen at the 2020 Olympic Games, but it is useful for the current discussion since there is evidence that testosterone influences sporting performance. Now let’s get to this high-school running competition.
Transgender athletes Terry Miller and Andraya Yearwood finished first and second in an in-door track competition. Miller’s time in the 55 m dash was 6.96 seconds; Yearwood’s time was 7.01 seconds; and the third place winner’s—a biological female—time was 7.23 seconds. Now, quite obviously, since the top-two placers times are, far and beyond, better than the third placer’s time, there is something strange about it. Since Miller and Yearwood are biological males, they have the anatomy and physiology of males since they were born males and went through male puberty. Miller and Yearwood also won competitions last year as well. Looking at their anatomy, compared to the women’s in the competition, how is that fair? That they went through male puberty and were exposed to higher levels of testosterone, how is that fair?
(From the Washington Times)
Look at the hips of the runner in red (a bio-male). Narrow hips are conducive to running success. This is because the quads run in a straight line from the hips, compared to a woman’s wider hips, where the quads sort of are on an angle. Another reason that wider hips are not conducive to running success—and why narrow hips are—is that women have what is called a wider Q-angle—or the quadriceps angle. Think of the average woman. Since they have wider hips, the angle for to their quads from their hips is wider. Males, obviously, have a narrower Q-angle, since they have narrower hips. Since they have narrower hips and therefore a narrower Q-angle, just on the basis of anatomy alone, we can say that, more often than not, men will blow women away in running—ceteris paribus.
You can even see what I mean just by looking at the above picture—there is a clear shot of the girl in yellow and how wide her hips are, although she is in motion.
Since males have narrower hips, then the quads almost go in a straight line, and since they are in the same line as the hips, they are in effect moving the same direction which does not impede running. Now, think of the Q-angle and how it is wider in women. Since the quads are not in-line with the hips, the quads need to do extra work in order to move the same distance as someone who has narrower hips. Women, compared to men, are less-efficient runners and this is due to their hip width and Q-angle.
Once puberty occurs is when the sexes really differentiate in both anatomy and physiology. This is due to the surge of testosterone increases in men, which cause harder bones, and is a driver of muscle growth. Testosterone stimulates red blood cell production (Beggs et al, 2014), which is important for work during a sprint, since the more blood that gets to a muscle, the harder that muscle can work. Women produce less testosterone. So, naturally, women will have less muscle than men. Even in men who “transition” to “women”—especially if they went through the male puberty—they will still have this advantage over them. A higher proportion of a man’s leg is muscle compared to women which can also help in running faster. Furthermore, since they have larger muscles and a higher percentage of their legs are muscle, then they necessarily would have higher amounts of type II muscle fibers which are conducive to sprinting success; sprinters are more likely to have fast-twitch (type II) muscle fibers in their vastus lateralis (Zierath and Hawley, 2004). (Also see Trappe et al, 2015 for a case-study on a world champion sprinter.)
Women have higher levels of estrogen than men; these higher levels of estrogen lead to higher body-fat percentage which then impedes running success. Higher levels of body-fat are not conducive to running speed/success because the body needs to work harder to move and, thusly, uses more energy to move since there is more weight—more fat—to move. Therefore, this is yet another reason why women are poorer runners than men.
Women have smaller, lighter lungs with fewer bronchioles than men at birth; boys have larger lungs than girls (Carey et al, 2008). Since women have smaller lungs than men, then, necessarily, women have a lower Vo2 max than men—meaning that women utilize less oxygen during exercise than men. The average Vo2 max for women is about 70-75 percent of that of males after puberty (Sharma and Kailashaya, 2016), while these differences in Vo2 max are still present even after correcting for muscle/fat mass (Stagner, 2009). So, the amount of oxygen that is produced during maximal exertion is greater for men; women have to work much harder than men to deliver more oxygen to their muscles to keep them going.
Women have smaller hearts (and smaller coronary vessels), which pump less blood per beat, meaning that their heart has to beat faster than a man’s to match a man’s cardiac output (Haward, Kalnins, and Kelly, 2001; Prabhavathi et al, 2014). Since women have smaller hearts, they have a smaller stroke volume—meaning the amount of oxygenated blood that the left ventricle releases is less than that of men who have bigger hearts and therefore bigger stroke volumes. Women have a higher heart rate than men (Lufti and Sukkar, 2011), but this is not enough to offset the lower stroke volume. Therefore, each time a woman’s heart pumps, it delivers less blood and oxygen to the muscles. Furthermore, women have 12 percent lower levels of hemoglobin than men (Murphy, 2014). Hemoglobin is a protein in the red blood cells (which women have fewer of) that transports oxygen to the blood. Since women have lower levels of hemoglobin and lower levels of red blood cells, then, less oxygen gets carried to the body’s tissues—muscles included.
I am a betting man and I would bet that both of those individuals who took first and second place in the competition in question would have beaten the women in all of the physiological variables that I have just discussed. We can outright see that the winner had extremely narrow hips. This is not to say that women who have narrow hips should not compete—but the fact of the matter is, that person has a whole slew of advantages over the women that he competed against because he went through male puberty.
What should be done here? There are three courses of action:
(1) Don’t let transgender athletes compete with women.
This is the most obvious course of action. Due to the anatomical and physiological differences between men and women that I described above, these types of people have an unfair advantage over women who did not go through the same type of puberty that they did. Now, one can make the same type of argument for Caster Semenya, who has been the subject of controversy the past few years, though, point (3) will address this.
(2) Have a separate competition for transgender athletes.
This seems to be a logical point. Just because people “identify” as something does not mean that they should compete in that competition. If someone identifies as disabled—even though they are not, physically, for instance—should they then be allowed to compete in the Special Olympics? Having separate competitions for these types of athletes would end these types of discussions—women who bust their ass year-round in order to succeed against their competition would not have to worry about competing against someone who went through a male puberty which would then throw out all of their hard training out the window.
(3) Separate individuals by anatomy and physiology.
This third and final point is separating individuals on the basis of anatomical and physiological parameters. Kerr and Obel (2017) compellingly argue that, instead of segregating sporting competitions by sex, sporting competitions should be segregated by anatomical and physiological parameters.
For example, take sprinting. Success in sprinting hinges on a few things: (1) muscle mass; the more muscle mass one has, especially in their legs, the more power they can generate in order to efficiently move; (2) fast twitch fiber count: the greater number of fast-twitch fibers in, for example, the vastus lateralis dictates how quick and explosive one can be. Coupled with the right morphology and fast-twitch fibers, this leads to more explosive contractions in RR genotypes (Broos et al, 2016). So we can say that for the 100m dash, it can be segregated on the basis of RR genotypes, an abundance of fast-twitch muscle fibers and a mesomorphic somatotype. So, if we know about what certain anatomic and physiologic variables are conducive in certain sporting events (we do know this) then segregating certain sports on the types of variables more conducive to success in that sport would lead to more balanced competition.
This would then end these types of arguments. Transgender athletes would then compete with individuals—male or female—on the basis of whichever anatomic and physiologic variables are conducive to the sport in question. The argument that Kerr and Obel advance is certainly intriguing—dare I say, it makes sense. Though it would take a lot to get it put into practice, it is an interesting thought experiment and makes more sense than just segregating based on sex alone.
Finally, Miller and Yearwood made some comments on their performance in that competition. When some of the girls said that it was unfair that they had to compete against people who went through male puberty, Miller said that the girls just need to “work harder” to compete with them [Miller and Yearwood]. This is ridiculous, due to what I outlined about the anatomic and physiologic differences between men and women. One of the competitors in the competition, Selina Soule said “We all know the outcome of the race before it even starts; it’s demoralizing.” Miller is the third fastest in the “women’s” (scarequotes due to the fact that it’s not all women anymore) 55-meter dash, while Yearwood is tied for 7th. These two should not be competing with women; they should either be competing with other transgender athletes or not competing at all.
In sum, we will be hearing a lot more about these types of things in the future. As more and more schools become “inclusive” to allow individuals who identify as X to compete in Y, there will be more and more outrage and then something would have to be done. I don’t see anything wrong with having them compete with other transgender athletes and only transgender athletes. Because then, the women who actually are women who train and bust their ass year-round to be the best they can be won’t be up-ended by men who walk onto the field who have anatomic and physiologic advantages who then blow them away (that much is clear by the time differences between the top two and third competitors in this competition).
Everyone wants to know the keys to athletic success, however, as I have argued in the past, to understand elite athletic performance, we must understand how the system works in concert with everything—especially in the environments the biological system finds itself in. To reduce factors down to genes, or training, or X or Y does not make sense; to look at what makes an elite athlete, the method of reductionism, while it does allow us to identify certain differences between athletes, it does not allow us to appreciate the full-range of how and why elite athletes differ in their sport of choice. One large meta-analysis has been done on the effects of a few genotypes on elite athletic performance, and it shows us what we already know (blacks are more likely to have the genotype associated with power performance—so why are there no black Strongmen or any competitors in the World’s Strongest Man?). A few studies and one meta-analysis exist, attempting to get to the bottom of the genetics of elite athletic performance and, while it of course plays a factor, as I have argued in the past, we must take a systems view of the matter.
One 2013 study found that a functional polymorphism in the angiotensinogen (ATG) region was 2 to 3 times more common in elite power athletes than in (non-athlete) controls and elite endurance athletes (Zarebska et al, 2013). This sample tested was Polish, n = 223, 156 males, 67 females, and then they further broke down their athletic sample into tiers. They tested 100 power athletes (29 100-400 m runners; 22 powerlifters; 20 weightlifters; 14 throwers and 15 jumpers) and 123 endurance athletes (4 tri-athletes; 6 race walkers; 14 road cyclists; 6 15 to 50 m cross-country skiers; 12 marathon runners; 53 rowers; 17 3 to 10 km runners; and 11 800 to 1500 m swimmers).
Zarebska et al (2013) attempted to replicate previous associations found in other studies (Buxens et al, 2009) most notably the association with the M235T polymorphism in the AGT (angiotensinogen) gene. Zarebska et al’s (2013) main finding was that there was a higher representation of elite power athletes with the CC and C alleles of the M235T polymorphism compared with endurance athletes and controls, which suggests that the C allele of the M235T gene “may be associated with a predisposition to power-oriented
events” (Zarebska et al, 2013: 2901).
Elite power athletes were more likely to possess the CC genotype; 40 percent of power athletes had the genotype whereas 13 percent of endurance had it and 18 percent of non-athletes had it. So power athletes were more than three times as likely to have the CC genotype, compared to endurance athletes and twice as likely to have it compared to non-athletes. On the other hand, one copy of the C allele was found in 55 percent of the power athletes whereas, for the endurance athletes and non-athletes, the C allele was found in about 40 percent of individuals. (Further, in the elite anaerobic athlete, explosive power was consistently found to be a difference maker in predicting elite sporting performance; Lorenz et al, 2013.)
Now we come to the more interesting parts: ethnic differences in the M235T polymorphism. Zarebska et al (2013: 2901-2902) write:
The M235T allele distribution varies widely according to the subject’s ethnic origin: the T235 allele is by far the most frequent in Africans (;0.90) and in African-Americans (;0.80). It is also high in the Japanese population (0.65–0.75). The T235 (C4027) allele distribution of the control participants in our study was lower (0.40) but was similar to that reported among Spanish Caucasians (0.41), as were the sports specialties of both the power athletes (throwers, sprinters, and jumpers) and endurance athletes (marathon runners, 3- to 10-km runners, and road cyclists), thus mirroring the aforementioned studies.
Zarebska et al (2013: 2902) conclude that their study—along with the study they replicated—supports the hypothesis that the C allele of the M235T polymorphism in the AGT gene may confer a competitive advantage in power-oriented sports, which is partly mediated through ANGII production in the skeletal muscles. Mechanisms can explain the mediation of ANGII production in skeletal muscles, such as a direct skeletal muscle hypertrophic effect, along with the redistribution of between muscle blood flow between type I (slow twitch) and II fibers (fast twitch), which would then augment power and speed. However, it is interesting to note that Zarebska et al (2013) did not find any differences between “top-elite” level athletes who had won medals in international competitions compared to elite-level athletes who were not medalists.
The big deal about this gene is that the AGT gene is part of the renin-angiotensin system which is partly responsible for blood pressure and body salt regulation (Hall, 1991; Schweda, 2014). There seems to be an ethnic difference in this polymorphism, and, according to Zarebska et al (2013), African Americans and Africans are more likely to have the polymorphisms that are associated with elite power performance.
There is also a meta-analysis on genotyping and elite power athlete performance (Weyerstrab et al, 2017). Weyerstrab et al (2017) meta-analyzed 36 studies which attempted to find associations between genotype and athletic ability. One of the polymorphisms studied was the famous ACTN3. It has been noted that, when conditions are right (i.e., the right morphology), the combined effects of morphology along with the contractile properties of the individual muscle fibers contribute to the enhanced performance of those with the RR ACTN3 genotype (Broos et al, 2016), while Ma et al (2013) also lend credence to the idea that genetics influences sporting performance. This is, in fact, the most-replicated association in regard to elite sporting performance: we know the mechanism behind how muscle fibers contract; we know how the fibers contract and the morphology needed to maximize the effectiveness of said fast twitch fibers (type II fibers). (Blacks have a higher proportion of type II fibers [see Caeser and Henry, 2015 for a review].)
Weyerstrab et al (2017) meta-analyzed 35 articles, finding significant associations with genotype and elite power performance. They found that ten polymorphisms were significantly associated with power athlete states. Their most interesting findings, though, were on race. Weyerstrab et al (2017: 6) write:
Results of this meta-analysis show that US African American carriers of the ACE AG genotype (rs4363) were more than two times more likely to become a power athlete compared to carriers of the ACE preferential genotype for power athlete status (AA) in this population.
“Power athlete” does not necessarily have to mean “strength athlete” as in powerlifters or weightlifters (more on weightlifters below).
Lastly, the AGT M235T polymorphism, while associated with other power movements, was not associated with elite weightlifting performance (Ben-Zaken et al, 2018). As noted above, this polymorphism was observed in other power athletes, and since these movements are largely similar (short, explosive movements), one would rightly reason that this association should hold for weightlifters, too. However, this is not what we find.
Weightlifting, compared to other explosive, power sports, is different. The beginning of the lifts take explosive power, but during the ascent of the lift, the lifter moves the weight slower, which is due to biomechanics and a heavy load. Ben-Zaken et al (2018) studied 47 weightlifters (38 male, 9 female) and 86 controls. Every athlete that was studied competed in national and international meets on a regular basis. Thirty of the weightlifters were also classified as “elite”, which entails participating in and winning national and international competitions such as the Olympics and the European and World Championships).
Ben-Zaken et al (2018) did find that weightlifters had a higher prevalence of the AGT 235T polymorphism when compared to controls, though there was no difference in the prevalence of this polymorphism when elite and national-level competitors were compared, which “[suggests] that this polymorphism cannot determine or predict elite competitive weightlifting performance” (Ben-Zaken et al, 2018: 38). Of course, a favorable genetic profile is important for sporting success, though, despite the higher prevalence of AGT in weightlifters compared to controls, this could not explain the difference between national and elite-level competitors. Other polymorphisms could, of course, contribute to weightlifting success, variables “such as training experience, superior equipment and facilities, adequate nutrition, greater familial support, and motivational factors, are crucial for top-level sports development as well” (Ben-Zaken et al, 2018: 39).
I should also comment on Anatoly Karlin’s new article The (Physical) Strength of Nations. I don’t disagree with his main overall point; I only disagree that grip strength is a good measure of overall strength—even though it does follow the expected patterns. Racial differences in grip strength exist, as I have covered in the past. Furthermore, there are associations between muscle strength and longevity, with stronger men being more likely to live longer, fuller lives (Ruiz et al, 2008; Volkalis, Haille, and Meisinger, 2015; Garcia-Hermosa, et al, 2018) so, of course, strength training can only be seen as a net positive, especially in regard to living a longer and fuller life. Hand grip strength does have a high correlation with overall strength (Wind et al, 2010; Trosclair et al, 2011). While handgrip strength can tell you a whole lot about your overall health (Lee et al, 2016), of course, there is no better proxy than actually doing the lifts/exercises to ascertain one’s level of strength.
There are replicated genetic associations between explosive, powerful athletic performance, along with even the understanding of the causal mechanisms behind the polymorphisms and their carry-over to power sports. We know that if morphology is right and the individual has the RR ACTN3 genotype, that they will exceed in explosive sports. We know the causal pathways of ACTN3 and how it leads to differences in sprinting competitions. It should be worth noting that, while we do know a lot more about the genomics of sports than we did 20, even 10 years ago, current genetic testing has zero predictive power in regard to talent identification (Pitsladis et al, 2013).
So, of course, for parents and coaches who wonder about the athletic potential of their children and students, the best way to gauge whether or not they will excel in athletics is…to have them compete and compare them to other kids. Even if the genetics aspect of elite power performance is fully unlocked one day (which I doubt it will be), the best way to ascertain whether or not one will excel in a sport is to put them to the test and see what happens. We are in our infancy in understanding the genomics of sporting performance, but when we do understand which genotypes are more prevalent in regard to certain sports (and of course the interactions of the genotype with the environment and genes), then we can better understand how and why others are better in certain sports.
The genomics of elite sporting performance is very interesting; however, the answer that reductionists want to see will not appear: genes are difference makers (Sterelny and Griffith, 1999), not causes, and along with a whole slew of other environmental and mental factors (Lippi, Favaloro, and Guidi 2008), along with a favorable genetic profile with sufficient training (and everything else that comes along with it) are needed for the athlete to reach their maximum athletic potential (see Guth and Roth, 2013). Genetic and environmental differences between individuals and groups most definitely explain differences in elite sporting performance, though elucidating what causes what and the mechanisms that cause the studied trait in question will be tough.
Just because group A has gene or gene networks G and they compete in competition C does not mean that gene or gene networks G contribute in full—or in part—to sporting success. The correlations could be coincidental and non-functional in regard to the sport in question. Athletes should be studied in isolation, meaning just studying a specific athlete in a specific discipline to ascertain how, what, and why works for the specific athlete along with taking anthropomorphic measures, seeing how bad they want “it”, and other environmental factors such as nutrition and training. Looking at the body as a system will take us away from privileging one part over another—while we also do understand that they do play a role but not the role that reductionists believe.
These studies, while they attempt to show us how genetic factors cause differences at the elite level in power sports, they will not tell the whole story, because we must look at the whole system, not reduce it down to the sum of its parts (Shenk, 2011: chapter 5). While blacks are more likely to have these polymorphisms that are associated with elite power athlete performance, this does not obviously carry over to strongman and powerlifting competition.
Due to evolving in different climates, the different races of Man have differing anatomy and physiology. This, then, leads to differences in sports performance—certain races do better than others in certain bouts of athletic prowess, and this is due to, in large part, heritable biological/physical differences between blacks and whites. Some of these differences are differences in somatotype, which bring a considerable advantage for, say, runners (an ecto-meso, for instance, would do very well in sprinting or distance running depending on fiber typing). This article will discuss differences in racial anatomy and physiology (again) and how it leads to disparities in certain sports performance.
Kerr (2010) argues that racial superiority in sport is a myth. (Read my rebuttal here.) In his article, Kerr (2010) attempts to rebut Entine’s (2000) book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It. In a nutshell, Kerr (2010) argues that race is not a valid category; that other, nongenetic factors play a role other than genetics (I don’t know if anyone has ever argued if it was just genetics). Race is a legitimate biological category, contrary to Kerr’s assertions. Kerr, in my view, strawman’s Entine (2002) by saying he’s a “genetic determinist”, but while he does discuss biological/genetic factors more than environmental ones, Entine is in no way a genetic determinist (at least that’s what I get from my reading of his book, other opinions may differ). Average physical differences between races are enough to delineate racial categories and then it’s only logical to infer that these average physical/physiological differences between the races (that will be reviewed below) would infer an advantage in certain sports over others, while the ultimate cause was the environment that said race’s ancestors evolved in (causing differences in somatotype and physiology).
Black athletic superiority has been discussed for decades. The reasons are numerous and of course, this has even been noticed by the general public. In 1991, half of the respondents of a poll on black vs. whites in sports “agreed with the idea that “blacks have more natural physical ability,“” (Hoberman, 1997: 207). Hoberman (1997) of course denies that there is any evidence that blacks have an advantage over whites in certain sports that come down to heritable biological factors (which he spends the whole book arguing). However, many blacks and whites do, in fact, believe in black athletic superiority and that physiologic and anatomic differences between the races do indeed cause racial differences in sporting performance (Wiggins, 1989). Though Wiggins (1989: 184) writes:
The anthropometric differences found between racial groups are usually nothing more than central tendencies and, in addition, do not take into account wide variations within these groups or the overlap among members of different races. This fact not only negates any reliable physiological comparisons of athletes along racial lines, but makes the whole notion of racially distinctive physiological abilities a moot point.
This is horribly wrong, as will be seen throughout this article.
|Data from Malina, (1969: 438)||n||Mesomorph||Ectomorph||Endomorph|
|Data from Malina (1969: 438)||Blacks||Whites|
|Thin-build body type||8.93||5.90|
|Submedium fatty development||48.31||29.39|
|Fat and very fat categories||9.09||21.06|
This was in blacks and whites aged 6 to 11. Even at these young ages, it is clear that there are considerable anatomic differences between blacks and whites which then lead to differences in sports performance, contra Wiggins (1989). A basic understanding of anatomy and how the human body works is needed in order to understand how and why blacks dominate certain sports over whites (and vice versa). Somatotype is, of course, predicated on lean mass, fat mass, bone density, stature, etc, which are heritable biological traits, thus, contrary to popular belief that somatotyping holds no explanatory power in sports today (see Hilliard, 2012).
One variable that makes up somatotype is fat-free body mass. There are, of course, racial differences in fat mass, too (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000). Lower fat mass would, of course, impede black excellence in swimming, and this is what we see (Rushton, 1997; Entine, 2000). Wagner and Heyward (2000) write:
Our review unequivocally shows that the FFB of blacks and whites differs significantly. It has been shown from cadaver and in vivo analyses that blacks have a greater BMC and BMD than do whites. These racial differences could substantially affect measures of body density and %BF. According to Lohman (63), a 2% change in the BMC of the body at a given body density could, theoretically, result in an 8% error in the estimation of %BF. Thus, the BMC and BMD of blacks must be considered when %BF is estimated.
While Vickery, Cureton, and Collins (1988) found that blacks had thinner skin folds than whites, however, in this sample, somatotype did not explain racial differences in bone density, like other studies (Malina, 1969), Vickery, Cureton, and Collins (1988) found that blacks were also more likely to be mesomorphic (which would then express itself in racial differences in sports).
Hallinan (1994) surveyed 32 sports science, exercise physiology, biomechanics, motor development, motor learning, and measurement evaluation textbooks to see what they said racial differences in sporting performance and how they explained them. Out of these 32 textbooks, according to Wikipedia, these “textbooks found that seven [textbooks] suggested that there are biophysical differences due to race that might explain differences in sports performance, one [textbook] expressed caution with the idea, and the other 24 [textbooks] did not mention the issue.” Furthermore, Strklaj and Solyali (2010), in their paper “Human Biological Variation in Anatomy Textbooks: The Role of Ancestry” write that their “results suggest that this type of human variation is either not accounted for or approached only superficially and in an outdated manner.”
It’s patently ridiculous that most textbooks on the anatomy and physiology of the human body do not talk about the anatomic and physiologic differences between racial and ethnic groups. Hoberman (1997) also argues the same, that there is no evidence to confirm the existence of black athletic superiority. Of course, many hypotheses have been proposed to explain how and why blacks are at an inherent advantage in sport. Hoberman (1997: 269) discusses one, writing (quoting world record Olympian in the 400-meter dash, Lee Evans):
“We were bred for it [athletic dominance] … Certainly the black people who survived in the slave ships must have contained the highest proportion of the strongest. Then, on the plantations, a strong black man was mated with a strong black woman. We were simply bred for physical qualities.”
While Hoberman (1997: 270-1) also notes:
Finally, by arguing for a cultural rather than a biological interpretation of “race,” Edwards proposed that black athletic superiority results from “a complex of societal conditions” that channels a disproporitionate number of talented blacks into athletic careers.
The fact that blacks were “bred for” athletic dominance is something that gets brought up often but has little (if any) empirical support (aside from just-so stories about white slavemasters breeding their best, biggest and strongest black slaves). The notion that “a complex of societal conditions” (Edwards, 1971: 39) explains black dominance in sports, while it has some explanatory power in regard to how well blacks do in sporting competition, it, of course, does not tell the whole story. Edwards (1978: 39) argues that these complex societal conditions “instill a heightened motivation among black male youths to achieve success in sports; thus, they channel a proportionately greater number of talented black people than whites into sports participation.” While this may, in fact, be true, this does nothing to rebut the point that differences in anatomic and physiologic factors are a driving force in racial differences in sporting performance. However, while these types of environmental/sociological arguments do show us why blacks are over-represented in some sports (because of course motivation to do well in the sport of choice does matter), they do not even discuss differences in anatomy or physiology which would also be affecting the relationship.
For example, one can have all of the athletic gifts in the world, one can be endowed with the best body type and physiology to do well in any type of sport you can imagine. However, if he does not have a strong mind, he will not succeed in the sport. Lippi, Favaloro, and Guidi (2008) write:
An advantageous physical genotype is not enough to build a top-class athlete, a champion capable of breaking Olympic records, if endurance elite performances (maximal rate of oxygen uptake, economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) (Williams & Folland, 2008) are not supported by a strong mental background.
Any athlete—no matter their race—needs a strong mental background, for if they don’t, they can have all of the physical gifts in the world, they will not become top-tier athletes in the sport of their choice; advantageous physical factors are imperative for success in differing sports, though myriad variables work in concert to produce the desired effect so you cannot have one without the other. On the other side, one can have a strong mental background and not have the requisite anatomy or physiology needed to succeed in the sport in question, but if he has a stronger mind than the individual with the requisite morphology, then he probably will win in a head-to-head competition. Either way, a strong mind is needed for strong performance in anything we do in life, and sport is no different.
Echoing what Hoberman (1997) writes, that “racist” thoughts of black superiority in part cause their success in sport, Sheldon, Jayaratne, and Petty (2007) predicted that white Americans’ beliefs in black athletic superiority would coincide with prejudice and negative stereotyping of black’s “intelligence” and work ethic. They studied 600 white men and women to ascertain their beliefs on black athletic superiority and the causes for it. Sheldon, Jayaratne, and Petty (2007: 45) discuss how it was believed by many, that there is a “ perceived inverse relationship between athleticism and intelligence (and hard work).” (JP Rushton was a big proponent of this hypothesis; see Rushton, 1997. It should also be noted that both Rushton, 1997 and Entine, 2000 believe that blacks’ higher rate of testosterone—3 to 15 percent— [Ross et al, 1986; Ellis and Nyborg, 1992; see rebuttal of both papers] causes their superior athletic performance, I have convincingly shown that they do not have higher levels of testosterone than other races, and if they do the difference is negligible.) However, in his book The Sports Gene: Inside the Science of Extraordinary Athletic Performance, Epstein (2014) writes:
With that stigma in mind [that there is an inverse relationship between “intelligence” and athletic performance], perhaps the most important writing Cooper did in Black Superman was his methodological evisceration of any supposed inverse link between physical and mental prowess. “The concept that physical superiority could somehow be a symptom of intellectual superiority became associated with African Americans … That association did not begin until about 1936.”
What Cooper (2004) implied is that there was no “inverse relationship” with intelligence and athletic ability until Jesse Owens blew away the competition at the 1936 Olympics in Berlin, Germany. In fact, the relationship between “intelligence” and athletic ability is positive (Heppe et al, 2016). Cooper is also a co-author of a paper Some Bio-Medical Mechanisms in Athletic Prowess with Morrison (Morrison and Cooper, 2006) where they argue—convincingly—that the “mutation appears to have triggered a series of physiological adjustments, which have had favourable athletic consequences.”
Thus, the hypothesis claims that differences in glucose conversion rates between West African blacks and her descendants began, but did not end with the sickling of the hemoglobin molecule, where valine is substituted for glutamic acid, which is the sixth amino acid of the beta chain of the hemoglobin molecule. Marlin et al (2007: 624) showed that male athletes who were inflicted with the sickle cell trait (SCT) “are able to perform sprints and brief exercises at the highest levels.” This is more evidence for Morrison and Cooper’s (2006) hypothesis on the evolution of muscle fiber typing in West African blacks.
Bejan, Jones, and Charles (2010) explain that the phenomenon of whites being faster swimmers in comparison to blacks being faster runners can be accounted for by physics. Since locomotion is a “falling-forward cycle“, body mass falls forward and then rises again, so mass that falls from a higher altitude falls faster and forward. The altitude is set by the position of center of mass above the ground for running, while for swimming it is set by the body rising out of the water. Blacks have a center of gravity that is about 3 percent higher than whites, which implies that blacks have a 1.5 percent speed advantage in running whereas whites have a 1.5 percent speed advantage in swimming. In the case of Asians, when all races were matched for height, Asians fared even better, than whites in swimming, but they do not set world records because they are not as tall as whites (Bejan, Jones, and Charles, 2010).
It has been proposed that stereotype threat is part of the reasons for East African running success (Baker and Horton, 2003). They state that many theories have been proposed to explain black African running success—from genetic theories to environmental determinism (the notion that physiologic adaptations to climate, too, drive differences in sporting competition). Baker and Horton (2003) note that “that young athletes have internalised these stereotypes and are choosing sport participation accordingly. He speculates that this is the reason why white running times in certain events have actually decreased over the past few years; whites are opting out of some sports based on perceived genetic inferiority.” While this may be true, this wouldn’t matter, as people gravitate toward what they are naturally good at—and what dictates that is their mind, anatomy, and physiology. They pretty much argue that stereotype threat is a cause of East African running performance on the basis of two assertions: (1) that East African runners are so good that it’s pointless to attempt to win if you are not East African and (2) since East Africans are so good, fewer people will try out and will continue the illusion that East Africans would dominate in middle- and long-distance running. However, while this view is plausible, there is little data to back the arguments.
To explain African running success, we must do it through a systems view—not one of reductionism (i.e., gene-finding). We need to see how the systems in question interact with every part. So while Jamaicans, Kenyans, and Ethiopians (and American blacks) do dominate in running competitions, attempting to “find genes” that account for success n these sports seems like a moot point—since the whole system is what matters, not what we can reduce the system in question to.
However, there are some competitions that blacks do not do so well in, and it is hardly discussed—if at all—by any author that I have read on this matter. Blacks are highly under-represented in strength sports and strongman competitions. Why? My explanation is simple: the causes for their superiority in sprinting and distance running (along with what makes them successful at baseball, football, and basketball) impedes them from doing well in strength and strongman competitions. It’s worth noting that no black man has ever won the World’s Strongest Man competition (indeed the only African country to even place—Rhodesia—was won by a white man) and the causes for these disparities come down to racial differences in anatomy and physiology.
I discussed racial differences in the big four lifts and how racial differences in anatomy and physiology would contribute to how well said race performed on the lift in question. I concluded that Europeans and Asians had more of an advantage over blacks in these lifts, and the reasons were due to inherent differences in anatomy and physiology. One major cause is also the differing muscle fiber typing distribution between the races (Alma et al, 1986; Tanner et al, 2002; Caesar and Henry, 2015 while blacks’ fiber typing helps them in short-distance sprinting (Zierath and Hawley, 2003). Muscle fiber typing is a huge cause of black athletic dominance (and non-dominance). Blacks are not stronger than whites, contrary to popular belief.
I also argued that Neanderthals were stronger than Homo sapiens, which then had implications for racial differences in strength (and sports). Neanderthals had a wider pelvis than our species since they evolved in colder climes (at the time) (Gruss and Schmidt, 2016). With a wider pelvis and shorter body than Homo sapiens, they were able to generate more power. I then implied that the current differences in strength and running we see between blacks and whites can be used for Neanderthals and Homo sapiens, thusly, evolution in differing climates lead to differences in somatotype, which eventually then lead to differences in sporting competition (what Baker and Horton, 2003 term “environmental determinism” which I will discuss in the context of racial differences in sports in the future).
Finally, blacks dominate the sport of bodybuilding, with Phil Heath dominating the competition for the past 7 years. Blacks dominate bodybuilding because, as noted above, blacks have thinner skin folds than whites, so their striations in their muscles would be more prevalent, on average, at the same exact %BF. Bodybuilders and weightlifters were similar in mesomorphy, but the bodybuilders showed more musculature than the bodybuilders whereas the weightlifters showed higher levels of body fat with a significant difference observed between bodybuilders and weightlifters in regard to endomorphy and ectomorphy (weightlifters skewing endo, bodybuilders skewing ecto, as I have argued in the past; Imran et al, 2011).
To conclude, blacks do dominate American sporting competition, and while much ink has been spilled arguing that cultural and social—not genetic or biologic—factors can explain black athletic superiority, they clearly work in concert with a strong mind to produce the athletic phenotype, no one factor has prominence over the other; though, above all, if one does not have the right mindset for the sport in question, they will not succeed. A complex array of factors is the cause of black athletic dominance, including muscle fibers, the type of mindset, anatomy, overall physiology and fat mass (among other variables) explain the hows and whys of black athletic superiority. Cultural and social explanations—on their own—do not tell the whole story, just as genetic/biologic explanations on their own would not either. Every aspect—including the historical—needs to be looked at when discussing the dominance (or lack thereof) in certain sports along with genetic and nongenetic factors to see how and why certain races and ethnies excel in certain sports.
Racial differences in sporting success are undeniable. The races are somewhat stratified in different sports and we can trace the cause of this to differences in genes and where one’s ancestors were born. We can then say that there is a relationship between them since, they have certain traits which their ancestors also had, which then correlate with geographic ancestry, and we can explain how and why certain populations dominate (or would have the capacity to based on body type and physiology) certain sporting events. Critiques of Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It are few and far between, and the few that I am aware of are alright, but this one I will discuss today is not particularly good, because the author makes a lot of claims he could have easily verified himself.
In 2010, Ian Kerr published The Myth of Racial Superiority in Sports, who states that there is a “dark side” to sports, and specifically sets his sights on Jon Entine’s (2000) book Taboo. In this article, Kerr (2010) makes a lot of, in my opinion, giant claims which provide a lot of evidence and arguments in order to show their validity. I will discuss Kerr’s views on race, biology, the “environment”, “genetic determinism”, and racial dominance in sports (which will have a focus on sprinting/distance running in this article).
Since establishing the reality and validity of the concept of race is central to proving Entine’s (2002) argument on racial differences in sports, then I must prove the reality of race (and rebut what Kerr 2010 writes about race). Kerr (2010: 20) writes:
First, it is important to note that Entine is not working in a vacuum; his assertions about race and sports are part of a larger ongoing argument about folk notions of race. Folk notions of race founded on the idea that deep, mutually exclusive biological categories dividing groups of people have scientific and cultural merit. This type of thinking is rooted in the notion that there are underlying, essential differences among people and that those observable physical differences among people are rooted in biology, in genetics (Ossorio, Duster, 2005: 2).
Dividing groups of people does have scientific, cultural and philosophical merit. The concept of “essences” has long been discarded by philosophers. Though there are differences in both anatomy and physiology in people that differ by geographic location, and this then, at the extreme end, would be enough to cause the differences in elite sporting competition that is seen.
Either way, the argument for the existence of race is simple: 1) populations differ in physical attributes (facial, morphological) which then 2) correlate with geographic ancestry. Therefore, race has a biological basis since the physical differences between these populations are biological in nature. Now that we have established that race exists using only physical features, it should be extremely simple to show how Kerr (2010) is in error with his strong claims regarding race and the so-called “mythology” of racial superiority in sports. Race is biological; the biological argument for race is sound (read here and here, and also see Hardimon, 2017).
True genetic determinism—as is commonly thought—does not have any sound, logical basis (Resnick and Vorhaus, 2006). So Kerr’s (2010) claims in this section need to be dissected here. This next quote, though, is pretty much imperative to the soundness and validity of his whole article, and let’s just say that it’s easy to rebut and invalidates his whole entire argument:
Vinay Harpalani is one of the most outspoken critics of using genetic determinism to validate notions of inferiority or the superiority of certain groups (in this case Black athletes). He argues that in order for any of Entine’s claims to be valid he must prove that: 1) there is a systematic way to define Black and White populations; 2) consistent and plausible genetic differences between the populations can be demonstrated; 3) a link between those genetic differences and athletic performance can be clearly shown (2004).
This is too easy to prove.
1) While I do agree that the terminology of ‘white’ and ‘black’ are extremely broad, as can be seen by looking at Rosenberg et al (2002), population clusters that cluster with what we call ‘white’ and ‘black’ exist (and are a part of continental-level minimalist races). So is there a systematic way to define ‘Black’ and ‘White’ populations? Yes, there is; genetic testing will show where one’s ancestors came from recently, thereby proving point 1.
2) Consistent and plausible genetic differences between populations can be demonstrated. Sure, there is more variation within races than between them (Lewontin, 1972; Rosenberg et al, 2002; Witherspoon et al, 2007; Hunley, Cabana, and Long, 2016). Even these small between-continent/group differences would have huge effects on the tail end of said distribution.
3) I have compiled numerous data on genetic differences between African ethnies and European ethnies and how these genetic differences then cause differences in elite athletic performance. I have shown that Jamaicans, West Africans, Kenyans and Ethiopians (certain subgroups of the two aforementioned countries) have genetic/somatypic differences that then lead to differences in these sporting competitions. So we can say that race can predict traits important for certain athletic competitions.
1) The terminology of ‘White’ and ‘Black’ are broad; but we can still classify individuals along these lines; 2) consistent and plausible genetic differences between races and ethnies do exist; 3) a link between these genetic differences between genes/athletic differences between groups can be found. Therefore Entine’s (2002) arguments—and the validity thereof—are sound.
Kerr (2010) then makes a few comments on the West’s “obsession with superficial physical features such as skin color”, but using Hardimon’s minimalist race concept, skin color is a part of the argument to prove the existence and biological reality of race, therefore skin color is not ‘superficial’, since it is also a tell of where one’s ancestors evolved in the recent past. Kerr (2010: 21) then writes:
Marks writes that Entine is saying one of three things: that the very best Black athletes have an inherent genetic advantage over the very best White athletes; that the average Black athlete has a genetic advantage over the average White athlete; that all Blacks have the genetic potential to be better athletes than all Whites. Clearly these three propositions are both unknowable and scientifically untenable. Marks writes that “the first statement is trivial, the secondly statistically intractable, and the third ridiculous for its racial essentialism” (Marks, 2000: 1077).
The first two, in my opinion (the very best black athletes have an inherent genetic advantage over the very best white athletes and the average black athlete has a genetic advantage over the average white athlete), are true, and I don’t know how you can deny this; especially if you’re talking about AVERAGES. The third statement is ridiculous, because it doesn’t work like that. Kerr (2010), of course, states that race is not a biological reality, but I’ve proven that it is so that statement is a non-factor.
Kerr (2010) then states that “ demonstrating across the board genetic variations between
populations — has in recent years been roundly debunked“, and also says “ Differences in height, skin color, and hair texture are simply the result of climate-related variation.” This is one of the craziest things I’ve read all year! Differences in height would cause differences in elite sporting competition; differences in skin color can be conceptualized as one’s ancestors’ multi-generational adaptation to the climate they evolved in as can hair texture. If only Kerr (2010) knew that this statement here was the beginning of the end of his shitty argument on Entine’s book. Race is a social construct of a biological reality, and there are genetic differences between races—however small (Risch et al, 2002; Tang et al, 2005) but these small differences can mean big differences at the elite level.
The “environment” and biological variability
Kerr (2010) then shifts his focus over to, not genetic differences, but biological differences. He specifically discusses the Kenyans—Kalenjin—stating that “height or weight, which play an instrumental role in helping define an individual’s athletic prowess, have not been proven to be exclusively rooted in biology or genetics.” While estimates of BMI and height are high (both around .8), I think we can disregard the numbers since they came from highly flawed twin studies, since molecular genetic evidence shows lower heritabilities. Either way, surely height is strongly influenced by ‘genes’. Another important caveat is that Kenya has one of the lowest BMIs in the world, 20.7 for Kenyan men, which also is part of the cause of why certain African ethnies dominate running competitions.
I don’t disagree with Kerr (2010) here too much; many papers show that SES/cultural/social factors are very important to Kenyan runners (Onywera et al, 2006; Wilbur and Pistiladis, 2012; Tucker, Onywera, and Santos-Concejero, 2015). You can have all of the ‘physical gifts’ in the world, if it’s not combined with the will to want to do your best, along with cultural and social factors you won’t succeed. But having an advantageous genotype and physique are useless without a strong mind (Lippi, Favaloro, and Guidi, 2008):
An advantageous physical genotype is not enough to build a top-class athlete, a champion capable of breaking Olympic records, if endurance elite performances (maximal rate of oxygen uptake, economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) (Williams & Folland, 2008) are not supported by a strong mental background.”
Dissecting this, though, is tougher. Because being born at certain altitudes will cause certain advantageous traits, such as a larger lung capacity (and you will have an advantage in lung capacity when competing at lower altitudes), but certain subpopulations live in these high-altitude areas, so what is it? Genetic? Cultural? Environmental? All three? Nature vs nurture is a false dichotomy; so it is a mixture of the three.
How does one explain, then, the athlete who trains countless hours a day fine-tuning a jump shot, like LeBron James or shaving seconds off sub-four minute miles like Robert Kipkoech Cheruiyot, a four time Boston Marathon winner?
Literally no one denies that elite athletes put in insane amounts of practice; but if everyone has the same amount of practice they won’t have similar abilities.
He also briefly brings up muscle fibers, stating:
These include studies on African fast twitch muscle fibers and development of motor skills. Entine includes these studies to demonstrate irrevocable proof of embedded genetic differences between populations but refuses to accept the fact that any differences may be due to environmental factors or training.
This, again, shows ignorance of the literature. An individual’s muscle fibers are formed during development from the fusion of several myoblasts, with differentiation being completed before birth. Muscle fiber typoing is also set at age 6, no difference in skeletal muscle tissue was found when comparing 6-year-olds and adults, therefore we can state that muscle fiber typing is set by age 6 (Bell et al, 1980). You can, of course, train type II fibers to have similar aerobic capacity to type I fibers, but they’ll never be fully similar. This is something that Kerr (2010) obviously is ignorant to because he’s not well-read on the literature which causes him to make dumb statements like “any differences [in muscle fiber typing] may be due to environmental factors or training“.
Black domination in sports
Finally, Kerr (2010) discusses the fact that whites dominated certain running competitions in the Olympics and that before the 1960s, a majority of distance-running gold medals went to white athletes. He then states that the 2008 Boston Marathon winner was Kenyan; but the next 4 behind him were not. Now, let’s check out the 2017 Marathon winners: Kenya, USA, Japan for the top 3; while 5 Kenyans/Ethiopians are in the top 15 while the same is also true of women; a Kenyan winner, with Kenyans/Ethiopians taking 5 of the top 15 spots. The fact that whites used to do well in running sports is a non-factor; Jesse Owens blew away the competition in the Games in Germany, which showed how blacks would begin to dominate in the US decades later.
Kerr (2010) then ends the article with a ton of wild claims; the wildest one, in my opinion, being that “Kenyans are no more genetically different from any other African or European population on average“, does anyone believe this? Because I have data to the contrary. They have a higher Vo2 max, which of course is trainable but with a ‘genetic’ component (Larsen, 2003), while other authors argue that genetic differences between populations account for differences in success in running competition between populations (Vancini et al, 2014), while male and female Kenyan and Ethiopian runners are the fastest in the half and full marathon (Knechtle et al, 2016). There is a large amount of data out there that speaks about Kenyan/Ethiopian and others’ dominance in running; it seems Kerr (2010) just ignored the data. I agree with Kerr that Kenyanholos show that humans can adapt to their environment; but his conclusion here:
The fact that runners coming from Kenya do so well in running events attests to the fact the combination of intense high altitude training, consumption of a low-fat, high protein diet, and a social and cultural expectation to succeed have created in recent decades an environment which is highly conducive to producing excellent long-distance runners.
is very strong, and while I don’t disagree at all with anything here, he’s disregarding how somatype and genes differ between Kenyans and other populations that compete in these sports that then lead to differences in elite sporting competitions.
Elite sporting performance is influenced by myriad factors, including psychology, ‘environment’, and genetic factors. Something that Kerr (2010) doesn’t understand—because he’s not well-read on this literature—is that many genetic factors that influence sporting performance are known. The ability to become elite depends on one’s capacity for endurance, muscle performance, the ability of the tendons and ligaments to withstand stress and injury, and the attitude to train and push above and beyond what normal people can do (Lippi, Longo, and Maffulli, 2010). We can then extend this to human races; some are better-equipped to excel in running competitions than others.
On its face, Kerr’s (2010) claim that there are no inherent differences between races is wrong. Races differ in somatype, which is due to evolution in different geographic locations for tens of thousands of years. The human body is perfectly adapted to for long distance running (Murray and Costa, 2012), and since our capabilities for endurance running evolved in Africa and they, theoretically, have a musculoskeletal structure similar to the Homo sapiens that left Africa around 70 kya, then it’s only logical to state that African’s, on average, have an inherent ability in running competitions (West and East Africans, while North Africans fare very well in middle distance running, which, again, comes down to living in higher altitudes like Kenyans and Ethiopians).
Wagner and Heyward (2000) reviewed many studies on the physiological differences between blacks and whites. Blacks skew towards mesomorphy; black youths had smaller billiac and bitrochanteric width (the widest measure of the pelvis at the outer edges and the flat process on the femur, respectively), and black infants had longer extremities than white infants (Wagner and Heyward, 2000). We have anatomic evidence that blacks are superior runners (in an American context). Mesomorphic athletes are more likely to be sprinters (Sands et al, 2005; which is also seen in prepubescent children: Marta et al, 2013) Kenyans are ecto-dominant (Vernillo et al, 2013) which helps to explain their success at long-distance running. So just on only looking at the phenotype (a marker for race with geographic ancestry, proving the biological existence of race) we can confidently state, on average just by looking at an individual or a population, how they will fare in certain competitions.
Kerr’s (2010) arguments leave a ton to be desired. Race exists and is a biological reality. I don’t know why this paper got published since it was so full of errors; his arguments were not sound and much of the literature contradicts his claims. What he states at the end about Kenyans is not wrong at all, but to not even bring up genetic/biologic differences as a factor influencing their performance is dishonest.
Of course, a whole slew of factors, be they biological, cultural, psychological, genetic, socioeconomic, anatomic, physiologic etc influence sporting performance, but certain traits are more likely to be found in certain populations, and in the year 2018 we have a good idea of what influences elite sporting performance and what does not. It just so happens that these traits are unevenly distributed between populations, and the cause is evolution in differing climates in differing geographic locations.
Race exists and is a biological reality. Biological anatomic/physiological differences between these races then manifest themselves in elite sporting competition. The races differ, on average, in traits important for success in certain competitions. Therefore, race explains some of the variance in elite sporting competition.
An opinion piece by sociologist Roslyn Kerr, senior lecturer in sociology of sport, from Lincoln University wrote an article on January 18th for The Conversation titled Why it might be time to eradicate sex segregation in sports where she argues against sex segregation in sports. She does publish articles on sports history, leisure studies and sports management and used to be a gymnast so she should have good knowledge—perhaps better than the general public—on anatomy and physiology and how they interact during elite sporting performances. Though is there anything to the argument she provides in her article? Maybe.
The paper is pretty good, though it, of course, uses sociological terms and cites feminist theorists talking about gender binaries in sports and how they’re not ‘fair’. One thing continously brought up in the paper is how there is no way to discern sex regarding sporting competitions (Simpson et al, 1993; Dickinson et al, 2002; Heggie, 2010), with even chromosome-based testing being thrown out (Elsas et al, 2000). which can be seen with the Olympics “still struggling to define gender“. They state that women are put through humiliating tests to discern their sex.
They use this to buttress their own arguments which are based off of what bodies of disables athletes did: whether or not one competed in a particular sport was not on their disability, per se, but the functionality of their own bodies. As an example, sporting bodies used to group people with, say, a similar spinal injury even though they had different physical abilities. Call me crazy, but I most definitely see the logic that these authors are getting at, and not only because I ruminated on something similar back in the summer in an article on transgendered athletes in sports, writing:
This then brings up some interesting implications. Should we segregate competitions by race since the races have strength and weaknesses due to biology and anatomy, such as somatype? It’s an interesting question to consider, but I think we can all agree on one thing: Women should compete with women, and men should compete with men. Thus, transgenders should compete with transgenders.
Of course I posed the question regarding different races since they have different strengths and weaknesses on average due to evolution in different environments. Kerr and Obel (2017) conclude (pg 13):
Numerous authors have noted that the current two-sex classification system is problematic. They argued that it does not include all bodies, such as intersex bodies, and more importantly, does not work to produce fair competition. Instead, some argued that other traits that we know influence sporting success should be used to classify bodies. In this article, we extended this idea through using the ANT concepts of assemblage and black box. Specifically, we interpreted the current understanding of the body that sex segregation is based on as a black box that assumes the constant superiority of the male body over the female. But we argued that with the body understood as an assemblage, this classification could be reassembled so that this black box is no longer given. Instead we argued that by identifying the multiple traits that make up the assemblage of sporting success, sex classification becomes irrelevant and that it is these traits that we should use to classify athletes rather than sex. Drawing on the example of disability sport we noted that the black box of a medical label was undone and replaced with an emphasis on functionality with different effects for each sport. This change had the effect of undoing rigid medical disability label and enabling athletes’ bodies to be viewed as assemblages consisting of various functional and potentially changing physical abilities. We used this discussion to propose a model of classified that eliminated the need for sex segregation and instead used physical measures such as LBM and VO2 capabilities to determine an athlete’s competitive class.
All of their other arguments aside that I disagree with in their paper (their use of ‘feminist theory’, gendered divisions, short discussions and quotes from other authors on the ‘power structure’ of males), I definitely see the logic here and, in my opinion, it makes sense. Anyway, those shortcomings aside, the actual argument of using anatomy and physiology and seeing which different parts work in concert to produce elite athletic performance in certain sports then having some kind of test, say, the Heath-Carter method for somatype (Wilmore, 1970) to a test of Vo2 max (Cureton et al, 1986) to even lean body mass (LBM).
Healy et al (2014) studied 693 elite athletes in a post-competition setting. They assesed testosterone, among other variables such as aerobic performance. They observed a difference of 10 of between men and women’s LBM and that it exclusively accounts for the “observed diffences in strength and aerobic performance seen between the sexes” while they conclude:
We have shown that despite differences in mean testosterone level between genders, there is complete overlap of the range of concentrations seen. This shows that the recent decision of the IOC and IAAF to limit participation in elite events to women with ‘normal’ serum testosterone is unsustainable.
Yes, this testosterone-influences-sports-performance is still ongoing. I’ve covered it a bit last year, and while I believe there is a link between testosterone and athletic ability and have provided some data and a few anecdotes from David Epstein, I do admit that the actual literature is scant with conclusive evidence that testosterone positively influences sport performance. Either way, if testosterone truly does infer an advantage then, of course, the model (which Kerr and Obel admit is simple at the moment) will need to be slightly revised. Arguments and citations can be found in this article written back in the summer on whether or not transgender MtFs should compete with women. This is also directly related to the MtF who dominated women a few months back.
Either way, the argument that once we better identify anatomic and physiologic causes for differences in certain sporting competition, this could, in theory, be used instead of sex segregation. I think it’s a good idea personally and to see how effective it could be there should be a trial run on it. Kerr and Obel state that it would make competition more ‘fair’. However, Sanchez et al, 2014 cite Murray (2010) who writes “fair sports competition does not require that athletes be equal in every imaginable respect.”
At the end of the day, what a lot of this rests on is whether or not testosterone infers athletic advantage at the elite level and there is considerable data for both sides. It’ll be interesting to see how the major sporting bodies handle the question of testosterone in sports and transgenders and hyperandrogenic females.
Personally, I think there may be something to Kerr and Obel’s arguments in their paper (feminist/patriarchy garbage aside) since it’s based on anatomy and physiology which is what we see on the field. However, it can also be argued that sex/gender is manifested in the brain which then infers other advantages/disadvantages in sports. Nonetheless, I think the argument in the paper is sound (the anatomy and physiology arguments only). For instance, we can look at one sport, say, 100 m dash, and we can say “OK, we know that sprinters have meso-ecto somatypes and that combined with the RR ACTN3 genotype, that confers elite athletic performance (Broos et al, 2016).” We could use those two variables along with leg length, foot length etc and then we can test—both in the lab and on the field—which variables infer advantages in certain sports. Another sport we can think of is swimming. Higher levels of body fat with wide clavicles and chest cavity are more conducive to swimming success. We could use those types of variables for swimming and so on.
Of course, this method may not work or it may only work in theory but not work in practice. Using lean body mass, Vo2 max etc etc based on which sport is in question may be better than using the ‘sex binary’, since some women (trust me, I’ve trained hundreds) would be able to compete head-to-head with men and, if for nothing else, it’d be good entertainment.
However, in my opinion, the logic on using anatomy and physiology instead of sex to segregate in sports is intriguing and, if nothing else, would finally give feminists (and non-feminists) the ‘equality’ they ask for.
Last year I bought The Genius in All of Us: New Insights Into Genetics, Talent, and IQ (Shenk, 2010) and while the book is interesting and I agree with a few things he says, he gets it horribly wrong on athleticism and ethnicity. Some of it I may be able to forgive since the book was written in 2010, but he does make some glaring errors. Chapter 6—pages 100-111—is titled Can White Men Jump? Ethnicity, Genes, Culture, and Success.
In the beginning of the chapter, Shenk writes that after the 2008 Beijing Summer Olympics, many articles were written about the Jamaican women who took the top three spots in the 100 and 200m races, with the emergence of Usain Bolt and his record-setting performance. Shenk (2010: 101) writes:
The powerful protein [alpha-actinin-3] is produced by a special gene variant called ACTN3, at least one copy of which is found in 98 percent of Jamaicans—far higher than in many other ethnic populations.
An impressive fact, but no one stopped to do the math. Eighty percent of Americans also had at least one copy of ACTN3—that amounts to 240 million people. Eighty-two percent of Europeans have it as well—that tacks on another 597 million potential sprinters. “There’s simply no clear relationship between the frequency of this variant in a population and its capacity to produce sprinting superstars,” concluded geneticist Daniel MacArthur.
I have written about MacArthur’s thoughts on the ACTN3 variant—that he helped discover, no less—in an article on Jamaicans, Kenyans, and Ethiopians and the explanatory factors in regard to their success in running competitions. Though, the article from MacArthur was written in 2008 and Shenk’s book was written in 2010, considerable advances have been made in this field. It was found that “combined effects of morphological and contractile properties of individual fast muscle fibers attribute to the enhanced performance observed in RR genotypes during explosive contractions” (Broos et al, 2016). Of course when talking about sprinting and morphology, you must think of the somatype. The somatype that is conducive to running success is a tall, lanky body with long limbs, as longer limbs can cover more distance. So European runners don’t have the right somatype, nor are the XX genotype for the ACTN3 variant high in Jamaicans (this genotype is present in ~2 percent of the Jamaican population; Scott et al, 2010). This—among other reasons I have laid out in the past—are why Jamaicans excel in sprinting competitions compared to other ethnic groups.
Shenk (2014: 10) further writes that sports success seem to come in ‘geographic clusters’, and the field of sports geography has been developed to understand it. “What they’ve discovered is that there’s never a single cause for a single cluster,” Shenk writes. “Rather, the success comes from many contributions of climate, media, demographics, politics, training, spirituality, education, economics and folklore. In short, athletic clusters are not genetic, but systemic.” Shenk then discusses the fact that these explanations are not good enough and that some ‘sports geographers’ have transformed themselves into ‘sports geneticists’ and then cites Jon Entine’s 2002 book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It where Shenk quotes Entine who quotes geneticist and physiologist Claude Bouchard who says that “these biological characteristics are not unique to West or East African blacks. These populations are seen in all populations, including whites” (Shenk, 2010: 102). Of course they’re not unique to one population and I don’t think that anyone has ever claimed that. Though the frequencies of these biological, morphological and physiological characteristics are not distributed evenly amongst populations and this explains how and why certain populations excel in certain sports when compared to others.
Shenk (2010: 102) also quotes Entine (2002), writing: “Entine also acknowledges that we haven’t actually found the actual genes he’s alluding to. “These genes will likely be identified early in the [twenty-first century],” he predicts.” We have ‘found some genes’ that aid in athletic performance, the ACTN3 genotype combined with type II fibers and the right morphology, as mentioned above for one. (Though a systems view—one of holism—makes much more sense here than a reducionist view. You must look at the whole system, not reduce things down, but that’s for another day.) That, in my opnion, is a large driver for ethnic differences in sports like this, because you need certain traits if you want to excel in these types of competitions.
He then discusses the success of the Kenyans in distance running—stating that 90 percent of Kenyan runners come from a small subset of Kenyans called the Kalenjin. He cites a few stories of some Kalenjin who talk about their experiences with no running water in their homes and that they had to “run to the river, to take your shower, run home, change, [run] to school . . . Everything is running” (Keino, a Kalenjin boy, quoted from Shenk, 2010: 104). Of course this is attributed to a multitude of factors, all of which have to work in concert to get the desired effect. For instance, sports psychologists have found that strong cultural achievement and the ability to work hard, compete, outdo others and seek new challenges drives their running dominance.
Shenk (2010: 106-107) then writes:
1.DESPITE APPEARANCES TO THE CONTRARY, RACIAL AND ETHNIC GROUPS ARE NOT GENETICALLY DISCRETE.
Skin color is a great deceiver; actual genetic differences between ethnic and geographic groups are very, very limited. All human beings are descended from the same African ancestors … [blah blah blah] … By no stretch of the imagination, then, does any ethnicity or region have an exclusive lock on a particular body type or secret high-performance gene. Body shapes, muscle fiber types, etc., are actually quite varied and scattered, and true athletic potential is widespread and plentiful.
Of course, I don’t think I have ever read anyone who denies this. However, as I’ve noted too many times to count, certain body types and muscle fiber distributions are more likely to be found in certain populations due to where their ancestors evolved recently, and so the fact that ‘actual genetic differences between ethnic and geographic groups are very, very, limited’ does not mean much when talking about dominance by a few populations in elite sporting competition. It just so happens to be the case that the somatypes and muscle fiber distributions that are conducive to running success are more likely to be found in populations of West and East African descent. This is an undeniable fact. (Also note how these ‘appearances to the contrary’ show how race is real.)
2.GENES DON’T DIRECTLY CAUSE TRAITS; THEY ONLY INFLUENCE THE SYSTEM.
Consistent with other lessons of GxE [Genes x Environment], the surprising finding of the $3 billion Human Genome Project is that only in rare instances do specific gene variants directly cause specific traits or diseases. …
As the search for athletic genes continues, therefore, the overwhelming evidence suggests that researchers will instead locate genes prone to certain types of interactions: gene variant A in combination with gene variant B, provoked into expression by X amount of training + Y altitude + Z will to win + a hundred other life variables (coaching, injuries, etc.), will produce some specific result R. What this means, of course, What this means, of course, is that we need to dispense rhetorically with thick firewall between biology (nature) and training (nurture). The reality of GxE assures that each persons genes interacts with his climate, altitude, culture, meals, language, customs and spirituality—everything—to produce unique lifestyle trajectories. Genes play a critical role, but as dynamic instruments, not a fixed blueprint. A seven- or fourteen- or twenty-eight-year-old is not that way merely because of genetic instruction. (Shenk, 2010: 107)
Nothing really wrong here. He is correct, which is why you need to look at the whole biological system, which also includes the culture, climate, environment and so on that the biological, developmental system finds itself in. However, Shenk then gets it wrong again writing that Jamaicans are a ‘quite heterogenous genetic group’ due to being a transport between North and South America. He states—correctly—that Jamaicans ancestry is about equal to that of African-Americans, but the individual variation in ancestry varies by “46.8 to 97.0 percent” (Shenk, 2010: 108).
Shenk gets a lot wrong here. For example. African-American and Jamaicans—despite both being descended from slave populations—have differing maternal ancestry which somehow influences athletic success. Deason (2017) found that 1) modern Jamaicans are descended from slaves and, who had considerable selective pressure on the population; 2) maternal ancestry could either influence sports success or be a false positive; 3) maternal lineages were different in Jamaicans and African-Americans, implying that the same maternal lineage is not distributed evenly between both sprinting populations; 4) some evidence exists that the genetic histories of Jamaicans and African-Americans are different based on their maternal haplotypes; 5) low SES and low access to healthcare—classic indicators of high African ancestry—were not directly linked to elite athletic success; 6) comparisons of the genomes of African-Americans and Jamaicans did not significantly differ since the estimated number of generations since admixture occurred, which implies that controls were not more likely to have more recent European ancestry than athletes; and 7) the regions of the genome that influence sprinting performance may be different in both populations. This is the best evidence to date against Shenk’s simplistic notions of the genetics between Jamaicans and African-Americans.
Differences in fast twitch fibers between Europeans and West Africans explain a large amount of the variance between Europeans and West African descendants in regard to sprinting success, while those with more symmetrical knees and ankles tend to run faster in the 100m dash (Trivers et al, 2014). This would also imply that Jamaicans have more symmetry in their knees and ankles than Europeans, though I am not aware of data that makes this comparison.
Shenk finally discusses the psycho-social-cultural aspects behind the phenomenon, stating that Roger Bannister, the first person to break the four minute mile, stated that while “biology sets limits to performance, it is the mind that plainly determines how close individuals come to those absolute limits” (Shenk, 2010: 110-111). Numerous psychological factors do, indeed, need to combine in order for the individual in question to excel in sports—along with the requisite anatomical/physiological/morphological traits too. Sasaki and Sekiya note that “changes in physiological arousal and movement velocuty induced by mild psychological pressure played a significant role in the sprint performance.” (See also Bali, 2015.)
Lippi, Favaloro, and Guidi, (2008) note how “An advantageous physical genotype is not enough to build a top-class athlete, a champion capable of breaking Olympic records, if endurance elite performances (maximal rate of oxygen uptake, economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) (Williams & Folland, 2008) are not supported by a strong mental background.” I have argued this for months, even if the beneficial somatype is there in the athlete in question, if he/she does not have the will to win they will not succeed in their goals. Psychosocial factors, of course, matter just as much as the physical but all of these factors work in concert to get the outcomes that occur in these sports.
Attempting to pinpoint one or a few traits—while it may help us to understand better physilogic and anatomic processes—tells us nothing about the entire system. This is why, for instance, the whole athletes system needs to be looked at—call it the ‘systems view of the athlete’, where all of these aforementioned variables work in concert to express elite athletic performance, with no one variable being higher than another as an explanatory factor in sports success. Though Shenk gets a few things right (like his point on genes not causing traits on their own, they just influence the system, and I’d take it a step further to note that genes are passive in their relationship to the physiological system as a whole and are only activated by the system as needed, not being ’causes’ on their own; Noble, 2008), he’s largely misguided on how certain aspects of Jamaican ancestry and morphology help propel them to running success in comparison to other ethnies.
When explaining elite athletic performance in certain areas of sports, you must take a view of the whole system, with each known variable influencing the next in the chain, if you want to explain why certain ethnies or racial groups do better in a given sport than other groups. A systems view is the only view to take when comparing populations in different athletic competitions. So the influence of culture, psychology, social effects, morphology, ancestry, anatomy, physiology, muscle fibers, etc all work in concert to produce elite athletic phenotypes that then excel in these sports, and reducing this down to certain variables—while it may help us understand some of the inner mechanics—it does nothing to help advance the hows and whys of elite success in sports competition when comparing different populations.
West Africans and their descendants have longer limbs and a shorter trunk than Europeans, on average—as I have extensively noted. Due to where they evolved, of course, they have a different morphology and physiology. Bergmann’s rule states that peoples with recent ancestry in the tropics will have slimmer pelvic bones and be narrower overall whereas Allen’s rule states that peoples with recent ancestry in the tropics will have long limbs, these traits being good for heat dissipation (Lieberman, 2015) and is one reason why West Africans and their descendants excel in these most sports in America.
The fact that a lot of African ethnic groups have different anatomic proportions and physiologic adaptations in comparison to people who have evolved in non-tropical climates is not contested. Morrison and Cooper’s (2006) hypothesis on sick cell anemia driving elite athletic performance in West Africans and their descendants is one of the most interesting explanations I’ve heard on the biochemical differences between the races. Sickle cell anemia is caused by a gene mutation. On amino acid 6, a single nucleotide substitution from A to T (As pair it Ts, Gs pair with Cs). This substitution changes a glutamic acid codon to valine codon which then causes sickling of the blood. Sickle cell anemia, of course, is not a ‘black disease’ as is popularly believed, but it, in fact, has to do with geography and the prevalence of malaria-carrying mosquitoes in that location. “This mutation“, Morrison and Cooper (2006) write “appears to have triggered a series of physiological adjustments, which have had favourable athletic consequences.”
Now, I’m aware that those who are already skeptical of this hypothesis may say ‘so does this mean that Italians, Greeks, MENA peoples etc have more type II fibers and would excel in these competitions?’, no it does not mean that because they don’t have the requisite morphology that West Africans have.
In the 1970s, a study was carried out on the physiological and anatomical proportions of Olympic athletes who competed in the 1968 Olympic games. Anatomic and physiologic measures were taken for each athlete. They used four racial classifications: Negroid, Caucasoid, Mongoloid, and mestizo (Indian/Spanish mix). The classifications were based on “were based on identification and somatotype photographs, as well as physical characteristics including skin color; general body shape; proportions of segments of the limbs; facial structure; form of eyes, lips, and nose; and colour and texture of hair” (Morrison and Cooper, 2006). This study, of course, also confirmed the anatomic differences between blacks and other races and how it leads to superior sports performance. Though, something peculiar was noted in the black athletes. Morrison and Cooper (2006) write: “Although the study failed to link athletic capability to a single gene system, the authors expressed “surprise” that “a sizeable number of Negroid Olympic athletes manifested the sickle-cell trait.””
One interesting study looked at the sickle cell trait (SCT) in French West Indian elite sprint athletes (Marlin et al, 2005). Using the French National Team for the year 2000, Marlin et al (2005) identified 3 sprinters (2 males and 1 female) who tested positive for the SCT. They also noticed a significantly higher presence of titles for people who tested positive for the SCT (38.6 percent for males and 50 percent for females. Marlin et al (2005: 624) conclude “that male SCT carriers are able to perform sprints and brief exercises at the highest levels” and “that brief and intensive exercise performance involving mainly alactic anaerobic metabolism may be enhanced by HbS in elite male sprinters.”
Blacks had narrower hips, longer arms and legs and a shorter trunk in comparison to other races. Of course, somatype is the variable that matters here but certain races are more likely to have certain anatomic characters that lead to superior spots performance on comparison to other races. The authors also attempted to link traits with single gene networks but were unsuccessful. However, they did notice that a large number of black athletes tested positive for the sickle cell trait. There is a conundrum here, however. People with the sickle cell gene might have a greater oxygen demand which causes more in vivo cell sickling. It was hypothesized that these individuals would be at a disadvantage since the 1968 Olympic games were held in Mexico city which is a high altitude area. They theorized that their blood would sickle more at the high altitude in comparison to low altitude but this was not seen.
Then another study was carried out which showed that not only do individuals with the sickle cell trait have lower hemoglobin levels, but all blacks do (Garn, Smith, and Clark, 1975). This is how and why they can perform at high altitudes despite having the sickle cell trait. Then, to test if this was mostly ‘environmental’ or ‘genetic’ they undertook a large study where they followed individuals throughout their whole lives and the difference persisted even later in life. Of course, according to other authors, some sort of compensatory mechanism should exist to counteract black’s lower hemoglobin levels, since this deficiency even exists in athletes (Morrison and Cooper, 2006).
As I’ve written about in the past, it was established that type I and type II fibers use different metabolic pathways and that type II fibers lead to improved athletic performance (along with the certain genotype for the ACTN3 gene). Morrison and Cooper (2006) also state that, of course, not all West Africans and descendants have this trait, and that these people came from a small area of West Africa.
A study looking at pulmonary differences between blacks and whites was conducted which found that blacks compensated for smaller lungs by breathing harder than whites while engaged in physical activity. In a study of 80 Asians and Europeans, Korotzer, Ong, and Hansen (2000) also showed that Asians had lower pulmonary functioning than Europeans. Even differences in chest size has been purported to explain differences in lung functioning, though this relationship did not hold (Whittaker, Sutton, and Beardsmore, 2005). Though, in his short review on race and the history of lung functioning, Braun (2015) writes that “At the very least, the idea that people labelled ‘white’ naturally have higher lung capacity than other races throughout the world should be approached with some skepticism.” because “Most commercially available spirometers internationally ‘correct’ or ‘adjust’ for race in one of two ways: by using a scaling factor for all people not considered to be ‘white’; or by applying population-specific norms. To enable the spirometer, the operator must select the race of an individual, as well as indicate their age, sex/gender and height. How race (or population) is determined varies, with most operators either asking patients to self-identify or ‘eyeballing it’. Interviews with users of the spirometer indicate that many operators are unaware that they are automatically activating race correction when they select a patient’s race (3). Because ‘correction’ is programmed into the spirometer by the manufacturer, it can be difficult to disable.”
Braun, Wolfgang, and Dickerson (2013) and Braun (2015) critiques pulmonary studies because in a large majority of cases, possible explanatory variables for lower lung functioning in black Americans could be related to SES. Harik-Khan, Muller, and Wise (2004) used participants from the Third National Health and Nutrition Examination Survey. They chose black and white children between the ages of 8 and 17 who did not smoke (n=1462, 623 whites and 839 blacks). Blacks were taller but had lower SES, had lower levels of vitamins A and C, along with lower levels of alpha carotene. They also had lower lung functioning. When they adjusted for confounds, sitting explained 42 to 53 percent of the racial difference, SES factors and antioxidant vitamin levels accounted for 7 to 10 percent of the difference. So they could only account for 50 to 63 percent of the difference. In 752 children aged 8 to 10 years of age, low birth weight accounted for 3 to 5 percent of the differences whereas maternal smoking had no effect (Harik-Khan, Muller, and Wise, 2004). So the remaining variation, obviously, will be accounted for by other SES variables, biology, or environmental factors.
Whitrow and Harding (2004) show that, at least for Caribbean blacks living in the UK, upper body differences explained most of the variation in lung functioning than did sitting height, with social correlates having a small but significant impact.
So because blacks have more type II fibers on average, they will convert glucose into energy more rapidly than whites. The energy for these muscle contractions comes from adenosine triphosphate (ATP). Blacks and whites both convert glucose into ATP for cellular functioning but in different ratios. These differences in muscular contractions driven by the metabolic pathway differences of the fibers are one large reason why blacks dominate sports.
Fibers are broken down into two types: fast and slow twitch. Slow twitch fibers use aerobic metabolism which is how they generate ATP and greater oxidative capacity due to higher levels for myoglobin. Oxygen bound to hemoglobin is carried to the red blood cells through capillaries that then influence muscular performance. Myoglobin is also essential for the transport of oxygen to the mitochondria where it is then consumed. Conversely, fast twitch fibers use anaerobic metabolism, have less oxidative capacity, less myoglobin and due to this, they are more dependent on anaerobic metabolism. Blacks also have “significantly higher levels of activity in their phosphagenic, glycolytic, and lactate dehydrogenase marbling pathways than their Caucasian counterparts” (Morrison and Cooper, 2006). This is where the production of ATP is regenerated,and so they have a huge advantage here. So higher faster production of ATP lead to more efficient ATP production, too. However when the ATP is depleted then it’s replaced by a reaction that depletes creatine phosphate. Skeletal muscle then converts “chemical energy into mechanical work” which only 30 to 50 percent is wasted as heat, so even small physiological differences can lead to large differences in performance (Morris and Cooper, 2006).
Though that’s not the only biochemical difference (faster ATP regeneration and production) between the blacks and whites that would explain sports performance. Morrison and Cooper (2006) write: “There is also considerably greater activity in the lactate dehydrogenase pathway of people of West African descent. A primary function of this pathway is to reduce muscle fatigue by converting lactic acid back to glucose and refeeding the muscles. This cyclic set of reactions, from muscles to liver and back to muscles, is known as the Cori cycle.”
Lactic acid production is that feeling in your muscles when during extended athletic activity whereas the postponement of muscle fatigue rests on the rate at which lactic acid is covered into glucose. The rate of this removal is further increased by the lactate dehydrogenase pathway describe above by Morrison and Cooper.
Clearly, the production of lactic acid causes problems during physical activity. The production of lactic acid into glucose to refers the muscles through the lactate dehydrogenase pathway is critical, for if glycogen reserves are depleted during extended physical activity then blood glucose would become the primary source of energy for the muscles, which could lead to lowered blood glucose levels and the nervous system may become compromised. During prolonged activity, however, if glucose isn’t available for energy then the body uses fat reserves which is less efficient than carbohydrates for energy and combustion.
Morrison and Cooper conclude: “Not the least of coincidence seems to be the influence of the compensatory sickle cell gene on oxygen transport and availability to the tissues. The reduced availability pulled with reduced oxygen myoglobin in the preponderant fast-twitch muscle fibres which are adapted for rapid anaerobic energy (ATP) regeneration, all give a new outcome of muscle anatomical and biochemical advantages which proffer a superior athleticism.”
Though, at the moment, as David Epstein states in his 2014 book The Sports Gene: Inside the Science of Extraordinary Athletic Performance, in a few studies done on mice genetically altered to have low hemoglobin levels, a there was a “shift of type IIa fast-twitch muscle fibers to type IIb “super fast twitch” muscle fibers in their lower legs” (Epstein, 2014: 179). This is also a developmental effect of mice in their lifetime, not a direct effect of evolution (Epstein, 2014: 179). No compensatory mechanism yet exists for humans, which I will attempt to untangle in future articles on the matter.
At the end of the chapter on this subject (Chapter 11, Malaria and Muscle Fibers, page 179), Epstein states that he asked physiologists their thoughts on the hypothesis. A few people approved of it, whereas one stated that he had evidence for physiological differences between blacks and whites that have not been studied before but he won’t release his results:
Several scientists I spoke to about the theory insisted they woud have no interest in investigating it because of the inevitably thorny issue of race involved. On of them told me that he actually has data on ethnic differences with respect to a particular physiological trait, but that he would never publish the data because of potential controversy. Another told me he would worry about following Cooper and Morrison’s line of inquiry because any suggestion of a physical advantage among a group of people could be equated to a corresponding lack of intellect, as if athleticism and intelligence were on some kind of biological teeter-totter. With that stigman in mind, perhaps the most important writing Cooper did in Black Superman [Cooper’s book] was his methodical eviseceration of any supposed inverse link between physical and mental prowess. “The concept that physical superiority could somehow be a symptomn of intellectual inferiority only developed when physical superiority became associated with African Americans,” Cooper wrote. “That association did not begin until about 1936.” The idea that athleticism was suddenly inversely proportional to intellect was never a cause of bigotry, but rather a result of it. And Cooper implied a more serious scientific inquiry into difficult issues, not less, is the appropriate path. (Epstein, 2014: 179) [Entine (2002) also spends a considerable amount of time debunking the myth of intelligence and athletic ability being negatively correlated in his 2002 book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It, which was kind of popularized by Rushton (1997) with his now debunked r/K selection theory.]
Things like this piss me off. These differences are actually measurable and lead to trait differences between the races, and know the mechanisms, pathways and whatnot and people are still. Scared to share their findings. One day, I hope, science will find a way to disregard people’s feelings in regard to people’s feelings on notable, testable and replicable differences between the races, most importantly between blacks and whites. I’ve noted how type II fibers lead to metabolic changes and small tears which then cause big problems. This is due to how fast the type II fibers fire in comparison to the slow twitch fibers.
This hypothesis is extremely interesting and now that I’ve laid out Morrison and Cooper’s (2006) hypothesis, I’m going to take a deep dive into this literature to see what I can prove about this hypothesis. Of course, the somatype along with the fiber distribution matters, as does having the XX genotype and not RR, which lends to superior athletic performance when coupled with type II muscle fibers (Broos et al, 2016). The pieces of this puzzle are, in my opinion, slowly being put together for someone to come along and integrate them into a coherent theory for the sickle cell trait and superior athletic performance through type II muscle fibers. It’s very interesting to note that elite sprinters were more likely to carry the SCT and that champion sprinters were more likely to have it too.
Back in July I wrote about how there is controversy on whether or not MtF transgenders should compete with ‘bio women’ and whether or not their anthropometry or hormones gave them an advantage over biological women (I am aware that T levels decrease once they go on HRT, just a lot of them still have T ranges in near the low end of the new numbers for men). Well I am reading The Sports Gene by Jerry Epstein and he brings up two (anecdotal) examples of MtF transgenders who take HRT and see a decrease in performance due to decreased T:
No scientist can claim to know the precise impact of testosterone on any individual athlete. But a 2012 study that spent three months following female athletes from a range of sports—including track and field and swimming—showed that elite-level competitors had testosterone levels that consistently remained more than twice as high as those of the nonelites. And there are powerful anecdotes as well.
Joanna Harper, fifty-five, is a medical physicist who was born a male and later transitioned to living as a woman. Harper also happens to be a nationally accomplished age-group runner, and when she started hormone therapy in August 2004 to suppress her body testosterone and physically transition to female [Note from RR: I, of course, do not agree with the use of ‘her’ and that ‘she’ ‘physically transition[ed] to female’] like any good scientist, she took data. Harper figured she would slow down gradually, but was surprised to find herself getting slower and weaker by the end of the first month. “I felt the same when I ran,” she says. “I just couldn’t go as fast.” In 2012, Harper won the U.S. national cross-country title for the fifty-five-to-fifty-nine age group, but age and gender-graded performance standards indicate that Harper is precisely as competitive now as a female as she was as a male. That is, as a female, Harper is just as good relative to women as she was relative to men before her transition, but she’s far slower than her former, higher-testosterone self.
In 2003, as a man, Harper ran Portland’s Helvetia Half-Marathon in 1:23:11. In 2005, as a woman, she ran the same race in 1:34:01. Harper’s male time was about fifty seconds faster than her female time. She has compiled data from five other runners who have transitioned from male to female, and all show the same pattern of precipitous speed decline. One runner competed in the same 5K for fifteen years straight, eight times as a man and then seven times as a woman following testosterone suppression therapy; always faster than nineteen minutes as a man, and always slower than twenty minutes as a woman. (Epstein, 2013: 78) [Keep in mind that I have the nook version so the physical copy may have this on a different page.
Yes this is anecdotal evidence that testosterone gave an advantage while ‘male’ and then when they ‘transitioned’ to ‘female’ it showed that they became weaker, but still at the top level of women’s performance. Knowing this—how this man had an advantage ‘as a man’ and kept the same relative advantage when he ‘transitioned to a woman’ is a large clue that testosterone does infer an inherent advantage to athletes who have more of the hormone surging through their body.
Testosterone is known to affect skeletal muscle growth, but the mechanisms by which testosterone affects muscle growth are not known (Bhasin, Woodhouse, and Storer, 2001). Also, women with very high androgen levels—whether it’s due to endogenous or exogenous testosterone—have a 2.5 to 5 percent advantage over women who have androgen levels in the normal range (Berman, 2017). So the difference in performance—between women at least—with high and low levels of testosterone is not too great, though that 2.5 to 5 percent advantage most likely would come into play at the very end of the race.
Also recall that I previously wrote that, per the IOC guidelines, a ‘MtF’ needs to ‘declare herself’ a woman for at least four years while taking HRT for 1-2 years to be able to compete with ‘the gender they think they are’. Well, the testosterone levels that the IOC states is ‘OK’ for ‘MtFs’ is still in the low range of the new testosterone guidelines for men! Testosterone most definitely does give an advantage in sports. Think of sports as a modern day test of survival. Basically, those good at sports—such as football and basketball for instance—would have been better able to form hunting parties in our evolutionary past. So while forming these parties, testosterone rose since testosterone raises while men are in groups as well as preparing for competition (Booth et al, 1989). So since our modern body plans sprang up around 2 mya with the appearance of Homo erectus in the fossil record, we can logically infer that cooperation and testosterone—among other things—were needed to be successful hunters.
So if you look at most sports as just a way for men to have a competitive spirit and simulate fighting/hunting with other men, then it makes it clear that testosterone does infer an advantage in sports. For instance, there is a clear relationship between testosterone and explosive jumping (Cardinale and Stone, 2006). These relationships are very clear, have large effects yet bodies like the IOC disregard these findings, allowing MtFs to compete with real women, even when the data and verbal argumentation against letting them compete are logically sound.
Studies do state, of course, that the relationship between high testosterone and athletic performance hasn’t been proven, they also haven’t been refuted either (Sudai, 2017). In fact, all you need to look at is traits that are influenced by testosterone—height, size of limbs, fat mass, shoulder width/size (the most androgen receptors lie in the shoulders and traps muscles, so to tell if someone is juicing, they will have low levels of body fat but ‘3-D delts’ and large traps) etc. So just by looking at a few simple traits and then comparing anatomy with females who have high testosterone compared to women who do not have high levels of testosterone, we can draw the logical conclusion that testosterone does increase sports performance for both men and women, and we have both anecdotal and experimental evidence for the assertion.
In sum, the anecdotal evidence from Epstein’s book is a good start. However, we will need more than anecdotal evidence to prove that testosterone truly does give individuals an advantage if they do have higher testosterone levels than their competition. As larger studies get done, these effects will begin to get teased out. I am certain that testosterone will be found to give a huge advantage in terms of sports, and since sports are a way for us to compete with each other, impress women, gauge other males’ fighting skills, and began as a way to hone skills used to hunt and fight (Lombardo, 2012). Sports began as a way for us to develop the skills needed to survive and hunt, among other things, and so, to hunt, you need to have high levels of testosterone to give that ‘boost’. So if sports began as a way to gauge potential rivals and allies, and as a way to hone/improve fighting skills, then we can logically state that testosterone does give an advantage in sports competition.
Much has been written about the genotypic and phenotypic differences in Jamaicans, Kenyans, and Ethiopians. Why do they dominate these competitions? Is it cultural? Genetic? Does training matter more? Grit? Expertise? There are multiple reasons that they have such an advantage, the most important one being their morphology/somatype. Of course other physiologic and morphologic factors come into play for these three populations, but the greatest physical advantage they have is their somatype which lends itself to running—whether short, medium or long distance.
Back in July, I argued that the wide-hipped Neanderthals were stronger than the recently migrated Homo sapiens, due mostly to pelvic anatomy (along with Neanderthal protein intake). That’s one of the keys to explaining African dominance in running: their long slender bodies with high limb ratios.
Kenyans and Ethiopians
Kenyan distance running is driven by an ethny named the Kalenjin, particularly of the Nandi tribe. Much research has been undertaken on the physiology and morphology of certain subpopulations of Kenyans, with a complex genotype, phenotype, and even SES interaction driving the dominance of this subpopulation (Tucker, Onywera, and Santos-Concejero, 2015). Another important factor is their low BMI. Kenyans have the lowest BMIs in the world at 21.5, which considerably helps in regards to distance running (Radovanovic et al, 2014; Shete, Bute, and Deshmukh, 2014; Sedeaud et al, 2015).
Kenyans—like Jamaicans and Ethiopians—dominate these competitions due to a complex interaction between genes, environment and SES (Tucker, Onywera, and Santos-Concejero, 2015). Though, of course, a lot of what makes certain Kenyan populations dominate is trainable in other populations. Caucasians can have similar trainability in regards to Vo2 max, oxidative enzymes, and running economy. However, Kenyans are more likely to be slender with longer limbs which is a huge advantage in these competitions. So having a good running economy and a high Vo2 max may be the primary causal factors that cause them to be so good at distance running, with, as I’ve noted in the past, a higher genetic ceiling for high Vo2 max, along with high-altitude training (Larsen, 2003). Though Saltin et al (1995) conclude that physical activity during childhood combined with intense training as a teenager explains the higher Vo2 max in Kenyan boys. Other factors such as low blood lactate and ammonia accumulation are also important.
Genetics, though, is the most likely explanation for African distance-running dominance (Vancini et al, 2014; see Scott and Pitsiladis, 2007 for alternative view that as of yet there are no genetic evidence for African running superiority).
Not all studies show that Kenyans have more slow-twitch (type I) fibers than Caucasians, though the oxygen cost of running at a given velocity was found to be lower in elite Kenyan runners compared to non-Kenyans, which may be due to body dimensions. Apparently, there is no indication that Kenyans possess a pulmonary system that confers a physiologic advantage over non-Kenyans (Larsen and Sheel, 2015). Ethiopian diets, however, met the most recommendations for macronutrients, but fluids were lacking (Beis et al, 2011), similar to what is found on similar studies in Kenyans (Onywera et al, 2003).
It is important to note that not all of the literature out there says that there are mainly physiologic/genetic reasons for their success in distance running; other factors that may be at play are somatype which leads to exceptional biomechanical and metabolic efficiency, high-altitude training, and the want to succeed for economic and social advancement (Wilbur and Pitsiladis, 2012). Oxygen transport of the blood doesn’t explain Kenyan dominance either, they have similar oxygen transport as elite German runners (Prommer et al, 2010). Though, women and men from Ethiopia and Kenya, although they only account for <0.1% of the marathons and half-marathons, achieved the fastest times and were the youngest in the half-marathons and full-marathons (Knechtle et al, 2016). Similar results were seen in Switzerland, with male Africans being faster and younger than non-Africans (Aschmann et al, 2013).
From the years 2000-2014, Knechtle et al (2017) analyzed the Boston, Berlin, New York, and Chicago marathon along with the Stockholm marathon. Over this time period, Ethiopian men improved their times, but Ethiopian women didn’t. Age increased in Ethiopian men, but not women. Female and male marathon runners from Ethiopia were the fastest (Knechtle et al 2017). More studies, though, are needed to unravel the complex relationship between environmental and genetic factors that cause East Africans to dominate distance running (Onywera, 2009). However, elite endurance athletes consistently test higher than non-elite athletes on running economy, Vo2 max, and anaerobic threshold (Lorenz et al, 2013), and mechanical work may be able to predict recreational long distance performance (Tartaruga et al, 2013).
Jamaican sprinting dominance has been chalked up to numerous factors, most recently, symmetry of the knees and ankles (Trivers, Palestis, and Manning, 2013; Trivers et al, 2014). Trivers et al (2014) write in the Discussion:
Jamaicans are the elite sprinters of the world. Why? If symmetry of knees and ankles is a factor, why should Jamaicans be especially symmetrical (there is no knowledge of whether they actually are)? One possibility is heterozygosity for genes important to sprinting. The slave trade greatly increased heterozygosity on the West African side by mixing genes up and down the West coast of Africa from Senegal to Nigeria , . Recently a mtDNA haplotype has been isolated that correlates with success in African American–but not Jamaican–sprinters . Since there is a general (if often weak) positive relationship between heterozygosity and body symmetry  we are eager to do targeted studies of genomics on areas associated with sprinting, including energy substrate utilization, muscle fibre-type distribution and body composition analyses (with specific reference to the shape and size of the glutei maximi). Fast twitch (anaerobic) muscle fibres are characterized by specific adaptations which benefit the performances of explosive high-intensity actions such as those involved in sprinting. Notably, West Africans appear to have a higher fast twitch muscle fibre content than do comparable Europeans (67.5% vs 59% in one sample , as cited in ).
It’s interesting to note that the mtDNA haplotype predicts success in African American sprinters, but not Jamaicans. In regards to mtDNA haplotypes, Jamaican sprinters had statistically similar mtDNA haplotypes, which suggests that the elite sprinters arose from the same source population which indicates that there is no population stratification or isolation on sprint performance. African American sprinters and non-sprinters, on the other hand, had statistically significant differences in mtDNA, which implies that maternal ancestry plays a part in sprinting performance (Deason et al, 2011). Studying both maternal and paternal haplotypes to see where source populations originate is important in these fields, since if we know where their population came from, then we can better understand the hows and whys of elite running performance—especially between race. Though demographic studies on Jamaicans show that elite sprinters come from the same demographic population, so genetics cannot possibly account for Jamaican sprinting success, so their sprinting success may be related to environmental and social factors (Irving et al, 2013). We know little about the genomics of elite sporting performance (Pitsiladis et al, 2013), so the physical correlates (somatype) and physiologic correlates will do for now.
Usain Bolt is the current fastest man in the world, due in part to his anthropometric advantage (Krzystof and Mero, 2013). As everyone knows, you cannot teach speed (Lombardo and Deaner, 2014). Bolt himself has a large advantage, in part, to his power development and biomechanical efficiency compared to the people he competes with (Beneke and Taylor, 2010). Though one study has noted that a human may be able to run faster quadrupedally than bipedally–stating that at the 2048 Olympic Games, that the fastest human on the planet may well be a quadrupedal runner (Kinugasa and Usami, 2016). One of the most important factors of acceleration in the 100m sprint is stride frequency (Mackala, Fostiak, and Kowalski, 2015).
In Afro-Caribbean adolescents, body height and stride number to body height ratio were the main determinants of sprint performance (Copaver, Hertogh, and Hue, 2012). Body height being a predictor of sprint performance is nothing new; taller people have longer limbs; longer limbs cover more distance per step. Indeed, sprinters are taller than the American population, there is more variability in men than in women, sprinters have lower body mass and the height range excludes people who are really tall or really short (Uth, 2005).
I will touch on fiber typing again since I’ve come across new information on it.
East Asians are less likely to have the RR allele of the ‘sprint gene’ (MacArthur and North, 2004) (ACTN3) while Bantus are more likely to have it. Alpha-actinen-3 is a skeletal muscle isoform which is encoded by the ACTN3 gene. Alpha-actinen-3 deficiency is common in the general population (North, 2008; Berman and North, 2010), which means that most people in the general population are XX. Eighteen percent of the population on earth is homozygous for this mutation (Ivarsson and Westerblad, 2015). This allele is the 577X allele, and Bantus are less likely to have it while Eurasians are more likely to have it. The frequency of the RR genotype is also highest in Bantus than in Asians (Mills et al, 2001). This is one very important reason why Eurasians are not faster than Africans (somatype matters too, of course).
Elite sprinters are more likely to be RR and less likely to be XX. Why does this matter? It matters because the RR genotype with the right morphology, fiber type (fast twitch) and contractile properties of the individual fast twitch fibers contribute to heightened performance with an RR genotype (Broos et al, 2016). Jamaicans are also less likely to have the XX genotype (~2 percent) along with Kenyans (Scott et al, 2010). So this shows that since Jamaicans are less likely to be XX, they’re more likely to be RR. So since XX i negatively associated with sprint status, then populations that have a lower frequency will be more likely to have more sprinters, whereas a population that has the genotype will have fewer sprinters.
This is one of many genetic factors that account for elite sprinting performance between populations. So, clearly, the right muscle fiber type combined with the right genotype from the ACTN3 gene infers an advantage, contrary to Daniel MacArthur’s claims that it does not (one of the authors of numerous studies on the ACTN3 gene).
The genetics of sprinting/distance running is currently poorly understood. Though we have a few candidates (and they’re really good, showing variation where they should) like the RR ACTN3 genotype combined with fast twitch fibers. This is very important to note. If you’re missing this, and you’re short with a low Vo2 max and low limb length, there’s an extremely high chance you will not be an elite sprinter/distance runner. I cannot emphasize enough how much the physical factors mean when it comes to this.
It is possible that SES variables combined with other psycho-social factors could explain why these three populations excel so well in these sports. Though, on the other hand, you cannot discount that the individual has to have the right somatype and physical capabilities first. Contrary to popular belief, fiber typing DOES give an advantage, especially if combined with other variables. Low BMI is very important, as are long limbs and a taller than average height.
When it comes to Jamaicans, symmetry of the knees and ankles help considerably, along with a low body mass and taller body. SES factors could be driving the will to compete in these three populations, however, the physical ability needs to be there first, then it needs to be nurtured. Over the next 5 to 10 years, we will have a better understanding of why some populations excel over others and that will largely be due to somatype, physiology, and genetic factors, with SES and other psycho-social factors driving the want to excel in the sport.
The physical differences that underlie the success of these three populations needs more study. Elite athletes of Jamaican, Kenyan, and Ethiopian descent need to be studied more to untangle the physiologic, psychological, physical and social factors that have them excel so well. We know that certain combinations of traits infer a great advantage in certain populations, we now just need enough elite athletes of these populations to study to see how and why they excel so much. The current body of research reviewed here is a good start, though it does leave some questions unanswered.