The concept of human variation in the ability to respond to exercise training was proposed almost 30 years ago. In a series of standardized and carefully monitored exercise training experiments conducted with groups of sedentary young men and women, 18–30 years of age, it was shown that there were large interindividual differences in the response to training, i.e., trainability.
Let’s begin with an example: Height, which is important for sports like basketball and volleyball, is estimated to be 80% heritable. This means that if you don’t have tall parents you probably won’t be an elite level athlete in those two sports. This data set also found that  genetic factors explained 59% of variation in body mass index and 50-60% in the strength measures. The main problem is that we don’t know which genes are responsible for changing performance.
In research, most of the genetic studies have focused on aerobic endurance, specifically using VO2max, which measures the maximal amount of oxygen you can utilize during an exercise test. The heritability of VO2max is about 50%. Muscle strength and power heritability is somewhere between 30-80% depending on the type of exercise.
The most comprehensive data on the individual differences in trainability come from the HERITAGE Family Study, in which 742 healthy but sedentary subjects followed a highly standardized, well-controlled, laboratory-based endurance-training programme for 20 weeks. The authors found that after adjustment for age, sex, baseline maximal oxygen uptake and baseline body mass and composition the heritability of the maximal oxygen uptake response to 20 weeks of standardized exercise training reached 47%. That’s not very much.
In science, we often use animals to do experiments. Several selection experiments have confirmed the concept that there is a substantial genetic component to the trainability of exercise performance traits. For instance, in one study on selection for high and low responses to treadmill training in rats, the mean running distance increase of the founder population was 222 meters (Troxell et al. 2003). Pairs of lowest and of highest responders to training were mated, and their offspring were later exposed to the same treadmill training programme. Offspring from the low line did not differ in trainability from the founders, while those from the high line improved their running distance by more than 60% over the low line. These results also revealed that the narrow heritability of running performance trainability reached 43% in rodents.
Moving back to humans, two of the most studied genes are angiotensin converting enzyme I (ACE I/D) and alpha-actinin 3 (ACTN3).
The ACE I/D polymorphism was the first genetic factor to be associated with human performance. The ACE gene codes for angiotensin-1 converting enzyme, part of the renin-angiotensin system responsible for controlling blood pressure by regulating body fluid levels. The I allele, which represents an insertion of 287 bp, is associated with lower serum and tissue ACE activity and improved performance in endurance sports. The deleted form of the variant (D allele) is associated with higher circulating and tissue ACE activity and enhanced performance at sports short bursts of power. The literature on the ACE allele is somewhat controversial, with a recent meta-analysis indicating that here was no statistically significant association between ACE I allele and endurance sport events, but measuring sport performance is difficult.
ACTN3 is a protein that helps muscles contract powerfully at high speeds. It has a polymorphism that leads to a premature stop codon (X) rather than an arginine (R) at position 577. The R allele is generally considered to be advantageous in power-oriented events, as the RR genotype is overrepresented in elite power athletes while the XX genotype is associated with lower sprinting ability and muscle strength. The idea is that in people who are lacking this protein, their muscles won't