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.