Ozzy Osbourne was curious and decided to have his genome sequenced.
“Given the swimming pools of booze I’ve guzzled over the years—not to mention all of the cocaine, morphine, sleeping pills, cough syrup, LSD, Rohypnol . . . you name it—there’s really no plausible medical reason why I should still be alive,” he said in the Sunday Times of London in 2010.
“Maybe my DNA could say why.”
What the now 69-year-old rocker found out was somewhat enlightening, but as with most examinations of individual traits, the results provided more hints than hard scientific conclusions.
Two clues may begin to explain the longevity enjoyed by the Prince of Darkness: a higher amount of a gene called ADH4, which helps break down alcohol, and small amounts of so-called Neanderthal genetic material, which may increase resilience to noxious environmental stimuli (Harmon 2010).
The DNA hints that might explain Ozzy’s longevity illustrate why we must consider individual variability in all aspects of the human condition before making blanket statements on health, fitness and nutrition. In Ozzy’s case, it isn’t a steady supplementation of bat heads that’s been keeping him alive—it is probably those testable genetic components combined with several environmental and genetic factors yet to be discovered.
Variability in Exercise and Diet Beyond Oz
Many factors contribute to individual responses to exercise and nutrition. Understanding these factors can help trainers and coaches better serve their clients and athletes.
First and foremost are genetic or heritable factors (specific genes from parents and grandparents) that form the foundation of our responses to exercise and diet. These factors help dictate height, body structure, overall strength, aerobic capacity and our response to specific nutrients in food. Other factors influence how these genes develop. A mother’s prenatal physical activity and nutrition, combined with her infant’s early childhood environment, are strong influences on the child’s overall genetics for body shape and training adaptations (Nuckols 2016).
Next up are epigenetic factors, which arise when our environment and lifestyle influence the expression or activation of specific genes. Epigenetic factors include weight training, sprint or long-distance running, dietary components, quality of sleep, and lifestyle stressors.
Balancing heritable and epigenetic factors can help to determine individual responses to specific workouts or diets. The key is for coaches, trainers, athletes and clients to understand clients’ innate strengths and to use the right epigenetic tools to take advantage of them.
Athletics have long been a laboratory for epigenetics, even if coaches haven’t always understood the underlying causes of a particular athlete’s achievement. Some factors are obvious: Athletes are either wired for speed, strength, quickness, endurance or some other innate trait—or they aren’t (see the sidebar “The Genetic Quirks of the World’s Top Athletes”). Other factors are more subtle, influenced by metabolism, bone structure, diet, gender (see the sidebar “Genetic Variability in Women”) and other things that vary from person to person.
Basic exercise physiology tells us that each person’s metabolism differs according to his or her muscle fiber contraction speed, the type of fuel used and how oxygen is utilized.
Aerobic metabolisms typically have slow-twitch contractile tissue (type I muscle fibers), fuel work with fat or blood lipids, and use more mitochondria to process oxygen for long-term activity. By contrast, anaerobic metabolisms have fast-twitch and more powerful contractile tissue (type IIa and IIb muscle fibers), fuel work with glucose or blood sugar, and have fewer mitochondria to deliver oxygen for energy, so they must depend primarily on internal chemical reactions for the fuel needed to keep muscle fibers contracting (Kenney, Wilmore & Costill 1999).
These metabolic processes are mostly genetic and can dramatically affect our response to different training modalities. Strength training and cardiovascular training studies show wide and varied responses beyond the primary conclusions, which usually represent the average of all responses. For instance, one distinct exercise protocol can produce muscle-size gains ranging from 0% to 54% in different participants (Hubal et al. 2005; Petrella et al. 2008).
Cardiovascular studies echo these results. The Heritage Study examined how 20 weeks of aerobic exercise training could improve cardiovascular and metabolic risk factors while boosting aerobic fitness. Subjects showed an average improvement of 400 milliliters of oxygen transported to the muscle per minute, but the range was huge—from 0 ml per minute to more than a liter per minute (Roth 2007).
Even high-intensity interval training, which has become the magic panacea of the decade, produces a wide spectrum of responses. A review of five studies found that 22% of participants failed to improve oxygen transport, 44% didn’t improve on a time-to-exhaustion test, and 50% didn’t improve their lactate threshold (Gurd et al. 2016).
Muscle fiber composition plays a role in deeper hormonal genetic responses to training. Levels of proteins like myostatin—which signals muscle growth to stop after a certain point—vary considerably. Low levels of myostatin can produce bigger muscles. Satellite cells (stem cells that repair and grow muscle after workouts or trauma damage) can exist in variable amounts and respond differently to strength training programming, increasing by as little as 0% or as much as 60% (Roth 2007; Petrella 2008).
These variations in strength and cardiovascular research mirror general estimates researchers have reached: 10%–15% of North Americans are highly dominant in aerobic metabolism, 10%–15% are anaerobic, and the remaining population is dispersed in varying percentages on the fast- and slow-twitch continuum (Bouchard, Malina & Perusse 1997).
Biomechanics and Bone Structure
While fiber types and hormonal responses remain mostly hidden from view, what we can see makes a huge difference. Body type, limb length, baseline muscle size and tendon location help determine how much weight we can lift, all other factors being equal.
Because movement results from applying force via a lever system around each joint, relative size of muscles and tendons can determine how much force can be exerted—we call this the muscle-to-tendon ratio. People with long muscles and short tendons can exert more force than their short-muscle, long-tendon counterparts. Somewhat logically, a favorable muscle-to-tendon ratio allows exertion of more force, creating greater potential for achieving larger muscles (Brzycki 2012). This means that clients with long-muscle bellies have the potential to be quite strong.
Where the tendon attaches to the bone relative to the joint is another subtle but important factor. The farther away a tendon’s attachment point is from a joint or fulcrum, the greater the biomechanical advantage and strength potential. This is much like sitting on a seesaw: The farther away from the fulcrum or center point of the seesaw you are, the easier it is to lift the person on the other side (Brzycki 2012).
Bone Length and Joint Shape
Bone length adds another biomechanical variable. In most areas of resistance training, thick chests and shorter torsos, legs and arms allow more weight to be lifted. Short legs and torsos and wide hips contribute to squat success, while adding long arms to the squat equation provides an advantage in the deadlift. These favorable variances mean higher weights move a shorter distance, creating a competitive advantage over those with longer torsos and limbs (Brzycki 2012).
A specific joint’s shape and mobility are further variables. Research on hip-flexion mobility found a range of 80–140 degrees of movement among 200 study participants. More range of motion allows us to squat to the floor and rest comfortably, while less mobility makes it tough to get in and out of chairs. More mobility also allows use of the hip joints and surrounding muscles for bending at the waist, whether it’s to do a deadlift or to pick up an object from the floor (Elson & Aspinall 2008; Krieger & Contreras 2017).
How the ball or head of the upper leg bone (femoris) is angled at its neck and how deeply it fits in the hip socket (acetabulum) contribute to many potential movement variances. The angle of the femoral neck can vary by 20 degrees or more, affecting how it fits into the acetabulum. The acetabulum’s depth and varying femoral-neck thicknesses also come into play, with a deep socket and thick neck limiting ROM, and a shallow socket and thin neck expanding it (Somerset 2015). Shoulder ball-and-socket joints are likely to have similar variabilities.
Diet and DNA
From a deep DNA standpoint, the main purpose of food is to provide energy and keep us functioning efficiently. Though taste, texture acquisition and packaging of food have evolved over the years, the essential survival function of food prevails.
The basic elements of food—fat, carbohydrate and protein—are macronutrients, or substrates that optimize the body’s ability to function. What percentages of each should be consumed have spawned much debate and confusion since the 1980s, the great low-fat/high-carbohydrate decade.
Twenty years later, no scientific evidence has surfaced to prove the health negatives attributed to fat, and now the debate has reversed, with high-fat/low-carb camps forming.
However, the truth is you can travel the globe and find populations surviving wonderfully on high-fat, low-fat, high-carb, high-dairy, all-meat or all-plant diets, with cultural and traditional diets based on a wide variety of whole foods (Pollan 2009).
Genes and Obesity
Though most lifestyle variables such as exercise, sleep and stress can explain variations in body composition and lean mass, researchers estimate that heritable factors drive about 50%–60% of body mass index. Roughly 185 genes implicated in obesity give some people a tendency to gain more weight than others living under similar circumstances (Scott-Dixon et al. 2017).
DNA-related factors that could be affecting people with obesity include the following:
- Repression or downregulation of certain energy pathways, such as those involved in breaking down fatty acids and amino acids.
- Lower levels of mitochondrial DNA in their fat tissue, which could partly explain metabolic problems such as fat storage in the liver, skeletal muscle and pancreas, instead of under the skin, resulting in insulin resistance.
- More copies of the FTO gene, associated with more body fat, higher weight and greater difficulty losing weight in populations ranging from North Americans to Asians. FTO’s full effects are not known.
Other weight-related genes are
- LEP, which is related to leptin, a hormone that senses how much stored fat we have;
- GHRL, related to ghrelin, a potent hunger stimulator; and
- DRD2, an influencer of dopamine, related to the neurobiological reward and decision-making pathways (which are also involved in addictions). In The Sports Gene (Current Publishing 2014), David Epstein makes the dopamine receptor connection in relation to activity levels (see the sidebar “Genetic Quirks of the World’s Top Athletes”), citing animal studies by Knab & Lightfoot (2010).
Genes also influence taste preferences, tolerance for certain foods (like dairy or wheat), how we process some nutrients, and how much we like sweet or fatty foods (Scott-Dixon et al. 2017).
Addressing Nutrition Variables
Diet books, web-based experts and celebrity health coaches pitch guaranteed nutritional cures because they worked for certain people. The problem is, what works for one may or may not work for someone else.
Furthermore, environmental and mental stressors, sleep patterns, and daily activity levels in response to exercise can influence eating patterns. In any case, most people lose weight by creating a daily caloric deficit—regardless of which diet they follow.
So what works? You must seek out answers through experimentation. Some clients respond well to an all-plant diet, while others need animal protein. Some respond to high-carb/low-fat eating, while others do the opposite. For all diets, there are five important questions to answer:
- If you are trying to lose weight, are you in a daily caloric deficit, and are you losing weight at a rate consistent with the deficit?
- Does your diet include the correct amounts of micronutrients (vitamins and minerals) to maintain healthy physiological functions like immune response?
- Are you effectively tracking intake to make sure it’s consistent with your goals?
- Do you have enough energy to perform daily workouts and your regular daily activities?
- Does the diet severely restrict certain substrates or nutrients like carbohydrate, fat or animal protein?
Obviously, answering yes to the first four questions says your nutritional choices are sound, while answering no suggests a need for adjustment. The fifth question is posed mainly to consider the effects of extreme dietary restrictions.
Even weight gain under sedentary conditions differs dramatically from person to person and can mostly be explained genetically.
Researchers from the Heritage Study mentioned earlier also studied weight gain by enrolling 12 pairs of twins in a 100-day experiment. The twins were overfed by 1,000 calories per day on 84 of the 100 days and remained sedentary for the entire experiment. Weight gain averaged 17.9 pounds but ranged from 9.5 to 29.3 pounds. Abdominal fat variability was also dramatic, ranging from no gain to a 200% increase (Bouchard, Malina & Perusse 1997).
Genetics and Programming
The vast multitude of variables affecting exercise and diet outcomes might make it seem impossible to design effective training programs without elaborate genetic tests, limb measurements, hormone panels or muscle biopsies—but it can be done. Genetic variables are simply another consideration for trainers and coaches interested in constructing programs that provide the most benefit to their athletes and clients.
And let’s be clear that factoring variability into programming is not an “excuse” for lack of achievement in areas like weight loss, strength gains or interval times. If Olympic sprint champion Usain Bolt had spent his early years training for the Olympic marathon and couldn’t place in the top 50 today, it wouldn’t be because he should’ve tried harder or found better coaches. It would be a failure to understand his individual response to endurance training.
This somewhat absurd example does demonstrate how you might explore the background of a potential client to find clues to training success. Clients with athletic histories, especially successful ones, can provide immediate information. Obviously, an overweight male client with a background in sprinting or explosive power sports would respond well to intensive weight training and high-intensity intervals. On the flip side, an overweight female client who was once a state high-school cross-country champion would be a candidate for more steady-state cardio and high-repetition strength training.
Clients with little or no athletic background may take a little longer to figure out, but you can monitor their responses to various training modalities to gauge success and progress. Six to 12 weeks of a specific strength or conditioning program with specific volume, frequency and work effort should yield significant improvement for someone who responds well to that modality. Little or no change means it’s time to try something else. The key is to make sure you have a wide variety of options for making significant adjustments.
Learn From Two Great Running Coaches
Running coaches Greg McMillan and Steve Magness provide excellent examples of adjusting training programs for endurance athletes to allow for the possibility that, even among long-
distance runners, muscle fiber composition may vary.
Fast-twitch-dominant athletes tend to automatically use more stored muscle glycogen than slow-twitch athletes. Because glycogen is a primary fuel of endurance efforts, training strategies for fast-twitch athletes should have more rest between intervals, lower tempos on tempo runs and less overall volume. Slow-twitch athletes can handle more volume, while blended-fiber types fall between the two other groups (McMillan 2016; Magness 2014).
McMillan and Magness have successfully coached recreational and national-ranked runners, and some research supports what they have intuited. In a study of 14 cross-country skiers, athletes who completed the previous year with standard endurance protocols of 84% low-intensity training and 16% high-intensity training were divided into a control group of athletes who had responded well to the training and an experimental group of athletes who had responded poorly. The control group repeated the previous year’s training program, while the experimental group doubled their high-intensity volume and reduced low-intensity training by 22%. This switch produced improvements in oxygen transport (VO2max), power output and overall competitive results in the experimental group (Gaskill et al. 1999). Results from runners and these cross-country skiers show that building a training program around individual and genetic strengths can drive noticeable improvements.
In addition to choosing the type of strength and conditioning programming, trainers and coaches need to weigh biomechanical variances when choosing exercises and critiquing technique. For instance, despite what you’ve learned about general technical standards for hip and shoulder exercises, full ranges of optimal motion should be adjusted based on each client’s specific ROM rather than a textbook or gym-rat version.
Unraveling the Genetic Code
A one-size-fits-one approach to training and coaching boils down to gathering more of the facts you need to do the most good for your clients and athletes in the limited time you spend together. It starts with recognizing the difference between heritable and epigenetic factors and understanding which factors have the greatest influence on a client’s training goals.
As science peels away more of the mysteries of DNA and athletic achievement every day, you can conduct your own experiments to figure out what works best for each of your clients. If you keep up with the research and ask clients the right questions about their family background and lifestyle habits, you’ll be able to provide the highly individualized training that generates referrals and improves the health of your business and career.
Bouchard, C., Malina, R., & Perusse, L. 1997. Genetics of Fitness and Physical Performance. Champaign, IL: Human Kinetics.
Brzycki, Matt. 2012. A Practical Approach to Strength Training. Indianapolis, IN: Cardinal Publishing.
Elson, R.A., & Aspinall, G.R. 2008. Measurement of hip range of flexion-extension and straight-leg raising. Clinical Orthopaedics and Related Research, 466, 281–86.
Epstein, D.J. 2014. The Sports Gene: Inside the Science of Extraordinary Athletic Performance. New York: Current Publishing.
Gaskill, S.E., et al. 1999. Responses to training in cross-country skiers. Medicine & Science in Sports & Exercise, 31 (8), 1211–17.
Gurd, B.J., et al. 2016. Incidence of nonresponse and individual patterns of response following sprint interval training. Applied Physiology, Nutrition, and Metabolism, 41 (3), 229–34.
Harmon, K. 2010. Ozzy Osbourne’s genome reveals some neanderthal lineage. Scientific American. Accessed Oct. 11, 2017: scientificamerican.com/article/ozzy-osbourne-genome/.
Henselmans, M. 2015. 9 Reasons why women should not train like men. Baysian Bodybuilding. Accessed Oct. 11, 2017: bayesianbodybuilding.com/why-women-should-not-train-like-men. Accessed August 2017.
Hubal, M.J., et al. 2005. Variability in muscle size and strength gain after unilateral resistance training. Medicine & Science in Sports & Exercise, 37 (6), 964–72.
Kenney, L.W., Wilmore, J.H., & Costill, D.L. 1999. Physiology of Sport and Exercise. Champaign, IL: Human Kinetics 1999.
Knab, A.M., & Lightfoot, T.J. 2010. Does the difference between physically active and couch potato lie in the dopamine system? International Journal of Biological Sciences, 6 (2), 133–50.
Krieger, J., & Contreras, B. 2017. Individual differences: The most important consideration for your fitness results that science doesn’t tell you. The Glute Guy. Accessed Oct. 11, 2017: bretcontreras.com/individual-differences-important-consideration-fitness-results-science-doesnt-tell/.
Magness, S. 2014. The Science of Running: How to Find Your Limit and Train to Maximize Your Performance. San Rafael, CA: Origin Press.
McMillan, G. 2016 The three running types: Do you know your type? McMillan Running. Accessed, Oct. 11, 2017: mcmillanrunning.com/runner-types-do-you-know-your-type/.
Nuckols, G. 2016 Genetics and strength training: Just how different are we? Accessed Aug. 14, 2017: strongerbyscience.com/genetics-and-strength-training-just-different/.
Petrella, J.K., et al. 2008. Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: A cluster analysis. Journal of Applied Physiology, 104 (6), 1736–42.
Pollan, M. 2010 In Defense of Food. New York: Penguin.
Roth, S.M. 2007. Genetics Primer for Exercise and Health. Champaign, IL: Human Kinetics.
Scott-Dixon, K., et al. 2017. Genetics: The Universe Within: Can Knowing More About Your Genes Help You Eat, Move, and Live Better? Toronto: Precision Nutrition.
Somerset, D. 2015. No two hips are the same. How anatomical variance can affect your range of motion. The Glute Guy. Accessed Oct. 11, 2017: bretcontreras.com/no-two-hips-are-the-same-how-anatomical-variance-can-affect-your-range-of-motion
Tiidus, P.M. 2007 Skeletal Muscle Damage and Repair. Champaign, IL: Human Kinetics 2007.
A research breakthrough increases the likelihood that sensors in smart workout clothes will soon provide valuable performance data.