In 1995, the Fat Free Mass Index (FFMI) study sought to determine an individual’s genetic muscular potential. The research was unusual in that it included anabolic steroid users as examples of people who had gone beyond their genetic potential.
The analysis was rife with problems, the most blatant of which was researchers defined genetic potential based on inclusion criteria from an earlier study. This was, “we advertised in four gymnasiums in the Boston, Massachusetts, area and in three gymnasiums in the Santa Monica, California area to recruit subjects. We offered $60 for a confidential interview to any male aged 16 years or older who had lifted weights for at least 2 years.”1
Think about two years of training at the age of sixteen. Is this when anyone reaches their genetic potential? Some people aren’t even finished with puberty by then.2 Also, consider the knowledge an average sixteen-year-old has. Do they train as optimally as a professional athlete? Do they get proper nutrition, or do they eat pizza and ice cream?
The FFMI was a disaster of a study, even from the author’s standpoint. “Admittedly, one cannot definitively diagnose steroid use simply on the basis of the FFMI, much as one cannot make a definitive diagnosis of alcohol intoxication in a man who displays ataxia and dysarthria (slurring of words) upon getting out of his automobile.”3
So can drug-tested athletes show us just how far our genetic potential can take us? Is the biggest difference in our genetics just how much anabolic hormones our bodies produce? The International Association of Athletics Federations recently made a decision on athletes with above normal testosterone as it applied to a particular female sprinter, Caster Semenya. She was barred from competition for having natural testosterone levels that are beyond what is considered normal for a female athlete.4 So we know the position of the anti-doping agencies is that athletes need to be in a normal range.
If substantial hormonal variation is not allowed in drug-tested sports, but almost no athletes are affected by this rule (Semenya’s case is extraordinarily unusual), then it would seem that the hormonal playing field is fairly level. So who really has an advantage?
The Actual Genetic Differences Between Athletes And Regular People
We regularly see people on social media dismissing the success of an athletic individual as just “good genetics.” This comment seems to be made most often by people lacking physical development. While it’s unfortunate so many people have been misled in fitness, it’s also easy to make excuses for failures or failed strategies. The reality is, there is no secret advantage you’re missing.
“Everyone’s taking performance-enhancing drugs” is an accusation we hear often. It’s usually made by internet commenters who likely train using an inefficient standard program and eat the standard US 70 percent plant-based nutrition (which is really just crackers, noodles, and pizza) and are frustrated by their lack of results. Statistics show only 6.6 percent of men over the age of eighteen in the United States take or have taken steroids/performance-enhancing drugs.5 And if only one percent of men are truly fit at all, that suggests at least six out of seven who use steroids and other drugs fail anyway. It’s clearly not the difference in fit versus unfit people.
Low myostatin has been cited as a contributing factor in genetic potential. However, these observations were made in humans with a rare myostatin mutation—you can count on one hand the people who have this worldwide. The only documented case of this mutation is in one child who has been under constant supervision for the sake of his cardiac health. His doctors are concerned that the excessive muscle mass could put too much of a strain on the cardiac system and end his life prematurely.6
Higher birth weight is statistically associated with greater strength later in life.7 Most likely, being born large and fed well as an infant contributes to becoming a bigger, stronger person as an adult. However, this finding does not take frame size into account. Being a taller or larger person with greater raw output doesn’t necessarily equate to a higher power-to-weight ratio.
Strength athletes and NFL players often have a unique genetic layout of their tendons, giving them more power capability than normal people even in the weaker range.8 As one study reports, “The location of a muscle’s tendon insertion into bone is another factor contributing to maximal strength expression. The distance from the joint center to the point of tendon insertion represents the moment arm of muscle force, or the effort arm. A tendon inserted slightly further away from the joint poses a mechanical advantage for force production…a powerlifter would benefit more from a larger moment arm of force. Tendon insertion is a genetic factor contributing to strength that does not change with training.”9 Another orthopedic study of this phenomenon states, “The tendon to bony insertion site varies dramatically along its length.”10
The longer the lever arm is from the point of insertion, the more the mechanical advantage for the creation of force (seen via electromyography and force measurement), the more opportunity to activate muscle during movement. There is no way to change this; it is simply genetic.11:
American football players are often seen as athletic strength athletes with diversity of skill—they can run fast and deliver force. The average NFL running back has a body weight of 232 pounds +/-18.7, and a percentage body fat of 16+/-4. The average NFL wide receiver has a body weight of 207.2 pounds +/-13.2, and a percentage body fat of 12.5+/-3.1.12: These measures were taken via DEXA scans, which show ~4 percent higher than standard skin fold measurements.13 14 15
What does this mean to X3 users? Because variable resistance off loads the weaker range of motion, the tendon factor becomes less relevant. This is also part of the reason for X3’s custom banding. We wanted the highest level of variance in force possible, not only to address differences between weak and impact-ready ranges, but to also level the playing field for individuals who have “poor genetics” in terms of a less advantageous tendon layout.
Pope, HG. Katz, DL. (1994). Psychiatric and Medical Effects of Anabolic-Androgenic Steroid Use: A Controlled Study of 160 Athletes. Arch Gen Psychiatry. 51(5):375–382. ↩︎
Kail, RV. Cavanaugh, JC. (2010). Human Development: A Lifespan View (5th ed.). Cengage Learning. p. 296. ↩︎
Kouri, E. M., Pope, J. H., Katz, D. L., & Oliva, P. (1995). Fat-free mass index in users and nonusers of anabolic-androgenic steroids. Clinical journal of sport medicine: official Journal of the Canadian Academy of Sport Medicine 5(4), 223-228. ↩︎
Burns, K. (2019, May 15). Caster Semenya and the Twisted Politics of Testosterone. Retrieved from https://www.wired.com/story/caster-semenya-and-the-twisted-politics-of-testosterone/. ↩︎
W. E. Buckley, C. E. Yesalis, 3rd, K. E. Friedl, W. A. Anderson, A. L. Streit, J. E. Wright. JAMA. (1988) Estimated prevalence of anabolic steroid use among male high school seniors; 260(23): 3441-3445. Anabolic steroid use by male and female middle school students. Pediatrics. 101(5): E6. ↩︎
Schuelke, M., Wagner, K. R., Stolz, L. E., Hübner, C., Riebel, T., Kömen, W., …& Lee, S. J. (2004). Myostatin mutation associated with gross muscle hypertrophy in a child. New England Journal of Medicine, 350(26), 2682-2688 ↩︎
Barr, J. G., Veena, S. R., Kiran, K. N., Wills, A. K., Winder, N. R., Kehoe, S., …& Krishnaveni, G. V. (2010). The relationship of birth weight, muscle size at birth and post-natal growth to grip strength in 9-year-old Indian children: findings from the Mysore Parthenon study. Journal of Developmental Origins of Health and Disease, 1(5), 329-337 ↩︎
Sewell, D., Griffin, M., & Watkins, P. (2014). Sport and exercise science: An introduction. Routledge. ↩︎
Ratamess, N. A. (2011). ACSM’s foundations of strength training and conditioning. Wolters Kluwer Health/Lippincott Williams & Wilkins. ↩︎
Thomopoulos, S., Williams, G. R., Gimbel, J. A., Favata, M., & Soslowsky, L. J. (2003). Variation of biomechanical, structural, and compositional properties along the tendon to bone insertion site. Journal of Orthopaedic Research, 21(3), 413-419. ↩︎
Wilson, A., & Lichtwark, G. (2011). The anatomical arrangement of muscle and tendon enhances limb versatility and locomotor performance. Philosophical Transactions of the Royal Society B: Biological Sciences, 366(1570), 1540-1553. ↩︎
Dengel, D. R., Raymond, C. J., & Bosch, T. A. (2017). Assessment of muscle mass. Body Composition: Health and Performance in Exercise and Sport. Boca Raton, FL: Taylor & Francis Group. ↩︎
Kamp, P. (2019, November 13). Body Fat Percentage Distribution for Men and Women in the United States. Retrieved February 3, 2020. ↩︎
Laurson, K. R., Eisenmann, J. C., & Welk, G. J. (2011). Body fat percentile curves for US children and adolescents. American Journal of Preventive Medicine, 41(4), S87-S92. ↩︎
Borrud, L. G., Flegal, K. M., Freedman, D. S., Li, Y., & Ogden, C. L. (2011). Smoothed percentage body fat percentiles for US children and adolescents, 1999-2004. ↩︎
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