Genetics clearly influence sprint performance—but by how much? There are several ways of answering this question. First, we can look for specific genetic variants that have an impact on performance. Second, we can estimate the heritability of speed or speed-related traits like muscular strength, height, and body type with twin and family studies. Finally, we can analyze the demographics of elite and sub-elite sprinters.
Most of the literature focuses on two specific mutations: the ACTN3 R557R/X and ACE I/D variants.
ACTN3 encodes the α-actinin-3 protein, which is mostly restricted to Type II (fast-twitch) muscle fibers. Humans with the ACTN3 557XX genotype have no α-actinin-3 at all, and in fact appear to have a higher proportion of Type I (slow-twitch) muscle fibers than ACTN3 557RX or ACTN3 557RR humans. The obvious hypothesis, then, is that 577RR athletes should be better sprinters than 577XX athletes because of the existence of α-actinin-3 and a higher proportion of fast-twitch muscle fibers.
This does in fact appear to be the case: a 2003 study found that out of 107 elite sprint/power athletes (sprinters ≤ 800m, swimmers ≤ 200m, track cyclists, speed skaters, and judo athletes), only 5.6% had the 577XX genotype, compared to 18.3% of a control group and 23.7% of a group of elite endurance athletes. Another study of 299 elite Japanese athletes found a significant difference between 577RR+RX athletes and XX athletes, with 100m times of 10.42 ± 0.05s for RR+RX athletes and 10.64 ± 0.09s for XX athletes. Finally, a 2016 multi-cohort study confirmed this research: of 255 “elite” Caucasian sprinters (defined as within 15% of the world record of 19.19s=22.07s), the average 200m time of 577RR athletes was significantly (p=0.016) faster than 577XX athletes. 577RX athletes were on par with 577 RR athletes, with a mean 200m time of 21.19 ± 0.53s for RR athletes and 21.29 ± 0.61s for RX athletes (and 21.86 ± 0.54 for RR athletes). More eye-openingly, “no Olympic-level sprinter has yet been identified with the 577XX genotype”. The same study concluded that the ACTN3 genotype explains 0.92% of sprint time variance.
The prevalence of the ACTN3 577XX genotype varies by ethnicity, but is overall relatively low: the highest incidence I could find was 25% 577XX for Asian populations. Other populations have lower incidences of the 577XX genotype, all the way down to African Bantu populations who are less than 1% 577XX.
Overall, it seems like 577RR and RX athletes appear to be better-suited for sprinting than 577XX athletes, but not necessarily by very much. Notably, even the XX athletes studied had fast times—certainly much faster than the average weekend warrior or even the average sprinter. While the XX genotype might keep an athlete from becoming an Olympic-level sprinter, it certainly doesn’t seem to limit athletes from achieving elite high school or even Division I times.
The ACE gene encodes the angiotensin-1 converting enzyme. Humans with the ACE-I variant have lower ACE levels than those with the ACE-D variant. I couldn’t find any information on how ACE levels might affect sprint performance.
That said, a study of British Olympic-standard athletes found that the frequency of ACE-I athletes tended to increase as the athlete’s distance increased: 62% of runners competing in the 5k and above had the ACE-I variant, while only 35% of sub-200m sprinters did (compared to 49% in a control group). A similar study of Russian athletes found an excess of ACE-D variants among short-distance athletes compared to a control group and medium- and long-disance athletes. And the same multi-cohort study from above found an association between ACE variants and speed, with ACE DD/DI athletes being significantly (p=0.001) faster than ACE II athletes over 200m, and that this association explained 1.48% of sprint time variance.
I could only find a single study measuring the prevalence of the ACE genotype across ethnic groups—it found that 24.7% of Caucasians had the ACE II genotype, compared to 82.8% of Samoans and 16.2% of Nigerians.
Like ACTN3, ACE seems to explain a very small amount of sprint time variance. Neither ACTN3 nor ACE seem to prevent an athlete from becoming very fast—although either variant might prevent athletes from becoming Olympic-caliber.
One study of 30m sprint times by pairs of twins with “similar healthy living habits” found that 85% of the variance in sprint time in women (and 67% of variance in men) was heritable. A less applicable study of mice found that heritability of mouse sprint running ranged from 17-33%.
Another approach to answering this question is by looking at variables that affect speed and estimating their heritability. For example, height, body mass, BMI, and explosive strength are all significantly correlated with sprint performance. These attributes are all somewhat heritable: this study found that genetic factors explain 81% of variation in height, 59% of variance in BMI, and 50-60% of variance in various measures of strength.
Of course, measures like height, BMI, and explosive strength are only weakly correlated with sprint speed. Extreme body types are relatively common in sprinting—compare Usain Bolt with Ben Johnson or Christian Coleman. It’s clear that while a certain level of muscularity and leanness is necessary to be elite, you can find success with almost any body type.
Perhaps unsuprisingly, I couldn’t find any research on the demographics of elite sprinters. That said, out of the 152 sprinters that have broken the 10-second barrier, the vast majority of them have been of West African descent: only three Caucasians and six Asians have broken the 10-second barrier. Certainly, if you go to any track meet in the United States, you’ll find that Asians are wildly under-represented.
While it doesn’t seem like an athlete’s ethnic group necessarily prevents them from achieving elite status, it’s telling just how over-represented West Africans are on the 100m all-time list.
So how much do genetics influence sprinting? At the elite and Olympic levels, genetics seem to play a larger role—for example, if you have the ACTN3 XX variant, it seems basically impossible that you’ll become an Olympic-level sprinter. Demographics tell a similar story, although with notable exceptions. Twin and family studies also seem to indicate that most measures of sprint speed are relatively heritable.
However, at a sub-elite level, genetics don’t seem to have very much impact at all: it seems possible for athletes with any genotype to achieve relatively fast (sub-11, sub-22) times. Diving into this research has definitely energized myself—I haven’t done any genetic testing, but my research indicates that no matter my genetic background, my current times are nowhere near my genetic ceiling.