The Sports Gene: Inside the Science of Extraordinary Athletic Performance

Chapter 5 opens with a five-page profile of Olympic runner Jim Ryun. It wasn’t until Ryun was in high school that he dedicated himself to training and made vast improvements in a short amount of time. Epstein offers up Ryun as an example of trainability, a quality that appears to be genetically present in some people and that allows for improvement with training way beyond the capacity of people without that genetic asset.

A 1992 project called HERITAGE that combined the forces of five universities in the United States and Canada sought to test how identical exercise regimens affected different people. The test group included groups of family members, an approach that allowed researchers to look at how DNA influenced results. Researchers used a metric of aerobic capacity, or “the amount of oxygen a person’s body can use when he or she is running or cycling all out” (80), to monitor a person’s aerobic improvement. In 2011, the HERITAGE group “identified twenty-one gene variants—slightly different versions of genes between people—that predict the inherited component of an individual subject’s aerobic improvement” (82). A further study revealed that “certain genes, though present in all subjects, were more or less active in highly trainable people compared with less trainable people” (83). In other words, some people are high responders, and others are low responders, to training.

Epstein tells a story from his own life about him and a Columbia University track teammate named Scott. Scott entered school a better runner than Epstein—he had a high baseline—but as the two men trained, Epstein made more drastic improvements, while Scott plateaued. This led to what Epstein now believes is a misconstruing of the genetic facts into moralistic judgments on the two runners: Scott was seen as a gifted athlete wasting his talent by not training hard enough, while Epstein was rewarded for overcoming his personal challenges through training. Epstein now believes both men trained in the exact same ways, with the likely difference being that Epstein is a genetic high responder.

One study of 1,900 young men found that six, termed the “naturally fit six” (91), had the aerobic capacity of collegiate runners despite having “no history of training whatsoever” (91). This demonstration of natural fitness, and the data about trainability, leads Epstein to investigate whether someone might have “elite-level aerobic endurance before training” (90). The journey and achievements of Chrissie Wellington, a British triathlete who won the Ironman World Championship in 2007 as a rookie after coming to the sport late in life, seems to be one example. Her story, complete with details of cycling effortlessly at high altitudes while practicing in Nepal, is full of evidence that she possesses a high baseline endurance.

The data of the “naturally fit six,” if extrapolated, would suggest that “there are more than 100,000 naturally fit people in the United States between the ages of twenty and sixty-five” (95). This figure leads Epstein to wonder “whether every professional endurance athlete in history might not have started as a member of the naturally fit fraternity” (95).

Epstein closes the essay with more evidence about genetic trainability: another story about Jim Ryun, who, when he gave up running and stopped training, saw his aerobic capacity decrease. Then, when he started training again, his aerobic capacity went back up to its exact levels from before he quit. 

Chapter 6 opens with a story about a newborn baby in Germany who was born with “bulging biceps.” This “Superbaby” piqued the interest of scientists who had formerly been studying a gene that produced “double muscle” in mice. That gene and its protein, both called myostatin, signal the stoppage of muscle growth. In the absence of that gene, animals (including humans) grow more muscle. Cows bred for more meat, whippets (a kind of dog) bred for racing, and thoroughbred racehorses all benefit from a myostatin mutation.

Scientists aim to use myostatin-based treatments for people with muscle-wasting diseases and in anti-aging therapies, but the prospect of building more muscle mass without genetic inhibitors is attractive to athletes, too. Geneticist Se-Jin Lee, who first identified the gene in mice, “is troubled by the apparent willingness of athletes to abuse technology that isn’t even technology yet, and that is meant for patients with no other options” (105).

Aside from genetic mutations, other genetic differences affect a person’s ability to build muscle mass. Satellite cells, or stem cells, that “swoop in to patch and build the muscle, bigger and better” (107) are one such difference. Studies measuring muscle growth demonstrated what the HERITAGE study revealed about endurance training: some people are high responders, and some are low. Furthermore, muscles are made of two types of fibers, fast-twitch and slow-twitch, and “some athletes have greater muscle growth potential than others because they start with a different allotment of muscle fibers” (109). Athletes with more fast-twitch fibers do better at sprinting sports, whereas athletes with more slow-twitch fibers do better at endurance sports.

On the topic of training, evidence suggests athletes “gravitate to and succeed in their sports because of how they’re already built” (110). Epstein adds, “both gene and fiber type data suggest that innate qualities of each individual ensure that there is no one-size-fits-all sport or method of training” (111). Athletes in sports like soccer, where all the members of the team train in the same way despite possessing different skills and genetic makeups, potentially suffer for this one-size-fits-all training.