How Much Do Genes Affect Your Athletic Potential?

Human genetics can play a major role in determining an athlete’s potential. Genetic information is passed from parent to child and is stored within human cells in the form of DNA (deoxyribonucleic acid). An individual’s DNA influences attributes such as height and weight and can help to determine if an individual has a predisposition towards athleticism. Genes play a major role in body type and athletic ability, but an athlete must also work hard to realize his/her potential.

Learn the basics of genes and athletic potential or read the more technical biological background.

Fast and Furious: How Muscle Fiber Type Influences Basketball Performance (Technical)


A unique combination of speed, agility, strength, and power sets professional athletes apart from the rest.  Are these attributes genetic, or do they result from hard work and dedication?  In science, answers are rarely black and white and this question is no different.  It is a complex interplay of genetics and training, which sets off a cascade of physiological and anatomical mechanisms, that produces our professional athletes.  These mechanisms are wide in their scope and intricate in their complexity.  Therefore, this article focuses on explaining muscle fiber properties in the context of basketball related performance.  It also presents some training principles to help the athlete improve his or her performance.

Muscles and Contractions 

When we decide to move a part of our body, the brain sends a signal through the nervous system. The signal, carried by motor neurons, then travels to the muscles required to perform the desired action, causing contraction and movement.  Despite this apparent simplicity, much more actually occurs, making this process quite complex.

The neuromuscular junction is the location where the signal from the nervous system meets the muscular tissue.  Motor neurons branch as they approach muscles to the point where only one individual branch innervates a muscle fiber (Seeley et al. 2006).  There is a small gap between the neuron and the fiber called the synaptic cleft.  The signal carried by the neuron causes a release of particles called neurotransmitters into the synaptic cleft, signaling the muscle fiber to fire (Seeley et al. 2006).

On the molecular scale, muscle contraction is a result of what is known as the sliding filament theory (Huxley and Hanson 1954, Huxley and Niedergerke 1954).  Briefly, each muscle fiber houses a sarcomere.  Inside the sarcomere, a thick filament composed of myosin and a thin filament composed of actin reside.   Upon neurotransmitter signaling, the thick myosin protein uses a ratchet motion to move the actin protein and cause contraction (Seeley et al. 2006, Plowman and Smith 2008).  A more in-depth explanation of the sliding filament theory and muscle contraction is given in another article: 95 miles per hour: Performance Physiology of Pitchers.

Muscle fibers are categorized into two groups: slow-twitch (ST) and fast-twitch (FT).  For the purposes of this article, we will consider the most common forms of these two fibers found in the literature.  Type I fibers are ST fibers and type II fibers are FT.  There are two classifications of type II fibers called type IIa and type IIx (Baechle and Earle 2008).  A surface level difference between fast- and slow-twitch fibers is the amount of blood supplied to the muscle.  Type I fibers have a well established blood supply and stain red during histochemical staining while type II fibers have a less developed blood supply and stain white (Zierath and Hawley 2004).  This can be seen in a chicken or turkey where breast meat is white (fast-twitch) and the legs and thighs are dark (slow-twitch).

Type I fibers have a small diameter with a large population of mitochondria, giving them a high aerobic capacity (Baechle and Earle 2008).  This aerobic capacity directly relates to the slow relaxation and twitch times, but also predisposes the muscle to fatigue slowly (Plowman and Smith 2008).  In physiology, structure always determines function.  The aforementioned structural characteristics give good evidence to say that type I fibers are used primarily in weak or moderately strong contractions that must take place over extended periods of time or that occur in a repetitive manner (MacIntosh et al. 2006).

Type IIx fibers are on the opposite end of the spectrum from ST fibers.  These fibers have a large diameter with a low density of mitochondria, thus, their aerobic capacity is low but their ability to function in the absence of oxygen is extremely high (Baechle and Earle 2008).  In stark contrast to ST fibers, type IIx fibers contract fast and hard but fatigue very easily (Plowman and Smith 2008).

In between type I and type IIx fibers are type IIa fibers.  These fibers are essentially a mix of the properties of the two extremes.  Their diameters could be considered intermediate in size and the density of mitochondria is at moderate levels as well (Baechle and Earle 2008).  They have the ability to work in oxygen rich and oxygen deprived situations, meaning they can function in long duration activities and those of shorter, more intense, effort as well (Plowman and Smith 2008).

So, does this information mean that when you want to go fast your body activates FT muscles and when you want to go slow it uses ST?  The answer to this is no: the body evokes a specific pipeline of recruitment to carry out all skeletal muscle tasks (MacIntosh et al. 2006).  The body starts with type I muscles, and then evokes type IIa in addition to type I as the need for contraction increases.  Finally, type IIx fibers can be recruited if the need for stronger contraction continues to grow (Vollestad et al. 1984, 1992, Vollestad and Blom 1985, Zajac and Faden 1985).  However, in specific fast or sudden corrective movements, the body does allow for type II units to be selectively activated (MacIntosh et al. 2006).  This phenomenon can be clearly seen in many reflexive actions.

The body’s specific protocol for muscle recruitment has implications for athletes.  If there are more ST muscles, it will take longer for the force of contraction to grow large enough to recruit more FT fibers.  Conversely, if there are fewer ST fibers, then type II fibers may be recruited sooner in those individuals.  Therefore, we will next look at the distribution of fibers within individuals and athletes.

The distribution of fiber types can vary from one person to another in the same group (Saltin et al. 1977) and depends on the genetics of individuals (Simoneau and Bouchard 1995).  However, scientists do have a general idea of locations in which each fiber type is in high density.  Muscles that contribute to sustained postural activity tend to have the highest amount of ST fibers (Plowman and Smith 2008), whereas the limbs contain more FT fibers (Seeley et al. 2006).  The percent of ST fibers in sprinters has been shown to be more than half that of endurance cyclists (Fox et al. 1993).  Furthermore, it has been shown that these differences can be attributed, to a degree, to sport specific exercise and training (Saltin et al. 1977).  What these data indicate is part of our distribution of fiber types is due to genetics, and some is due to sport-specific training.

Basketball’s Physiological Requirements 

Understanding the training needs for basketball requires more than just knowing about muscle fiber types.  It requires a thorough knowledge of the systems needed during competition.  Therefore, this section will briefly discuss the muscles, energy systems, and recovery principles that contribute to speed, agility, and power on the basketball court.

The upper body demands of a basketball player are greatly inferior to those of the lower body.  For this reason, the focus will be on the lower body only.  The buttocks, quadriceps, hamstrings, and calves play the most significant role in speed, agility and power.  Core stability has been shown to contribute to running performance (Sato and Mokha 2009), so it must be considered as well.

A study done by McInnes et al. (1995) sought to quantify the physiologic load placed on basketball players, lending insight into training demands for athletes.  They found that players change direction on average every 2.0 seconds.  Additionally, they did about 105 high-intensity sprints per game, one every 21 seconds, lasting an average of 1.7 seconds.  Data indicate glycolysis as the primary energy producer, meaning that anaerobic endurance is required.  Furthermore, players had an average heart rate of about 169 beats per minute throughout the game.  All these data led the authors to conclude that metabolic and cardiovascular demands are high in basketball players (McInnes et al. 1995).

Fitness and Training 

It is important to review the needs and goals of a training program designed around a basketball player.  First and foremost, the program must train for FT fiber development in the legs.  At the same time, the anaerobic energy system must be trained to ensure stamina and recovery during high intensity bursts.  Finally, agility (which is the ability to change direction) needs to be incorporated.

Agility training has been shown to increase muscular response times in the quadriceps and gastrocnemius (calves) (Wojtys et al. 1996).  T-drills, lateral movement drills, and balance drills are all components of agility training.  The type and variety of agility drills is endless, essentially any drill that incorporates quick movements with changes in direction in 5-15 second intervals will improve agility, build anaerobic endurance, and develop FT fibers.

Plyometric (plyos) and ladder drills are two effective means of increasing quickness and explosiveness through FT fiber development.  Plyos are generally very rapid, short distance jumps that occur in 5-20 second sets.  Dot drills and four-square setups are the most common.  In both, there is a pattern of dots or numbers on the ground in which the athlete uses one or two legs to hop about the pattern in a variety of ways.  Speed ladders are similar but all movements move the athlete along the ladder, making these drills less stationary.  These two methods are nearly endless in their variety.

Incorporating core training must be done as well.  Swiss ball, stabilization, lower back, and hip flexor exercises work together to build the entire core.  We have discussed that the stabilizing core muscles are primarily ST fibers, so exercises need to be designed with this in mind.  Rapid repetitions are less important here as the body is genetically predisposed to maintain ST fibers in this region (Plowman and Smith 2008).  Long duration core stabilization exercises like leg raises and planks should be the focus.

Finally, it is important to work the training protocol around the previously mentioned activity data from McInnes et al.  These data tell how to design recovery times between sets and between training sessions.  Recovery should never be taken lightly as it is just as important as the actual activity in improving performance.


The principles presented in this article can be applied to a wide range of sports whose demands are similar to those of basketball.  It is important to remember that there are limits to everyone’s abilities.  Most of us will never get close to the level of Michael Jordan or LeBron James, yet each person does have room to improve in some aspect of their game.  The requirements for improvement are simple: hard work and dedication.  With these two ideas in mind, it is nearly impossible to produce a training program that does not improve performance.


By: Josh Silvernagel, Graduate Student, Bioengineering, University of Utah
Josh Silvernagel received undergraduate degrees in Exercise Science and Mathematics from Bemidji State University (BSU) in Bemidji, MN.  During his undergraduate studies, he was a four year starter in baseball for the BSU Beavers, where he both pitched and played infield.  In addition to providing sport specific training for ametuer and professional athletes following school, Josh spent two years coaching the sport at both the collegiate and high school levels.  He is currently working on a Ph. D. in Bioengineering at the University of Utah, where he studies cardiac electrophysiology in the CARMA Center.  Josh and his wife, Danielle, are recently married.


Baechle, T. R., and R. W. Earle (Eds.). 2008. Essentials of Strength Training and Conditioning, 3rd edition. Human Kinetics, Champaign, IL.

Fox, E. L., R. W. Bowers, and M. L. Foss. 1993. The Physiological Basis for Exercise and Sport. Pages 94–135. Brown & Benchmark, Dubuque, IA.

Huxley, A. F., and R. Niedergerke. 1954. Structural changes in muscle during contraction: Interference microscopy of living muscle fibres. Nature 173:971–973.

Huxley, H., and J. Hanson. 1954. Changes in the cross-striations of muscle during contraction and stretch and thier structural interpretation. Nature 173:973–976.

MacIntosh, B. R., P. F. Gardiner, and A. J. McComas. 2006. Skeletal Muscle: Form and Function, 2nd edition. Human Kinetics, Champaign, IL.

McInnes, S. E., J. S. Carlson, C. J. Jones, and M. J. McKenna. 1995. The physiological load imposed on basketball players during competition. Journal of Sports Sciences 13:387–397.

Plowman, S., and D. Smith. 2008. Exercise Physiology for Health, Fitness, and Performance, 2nd edition. Kippincott Williams & Wilkins, Philadelphia, PA.

Saltin, B., J. Henriksson, E. Nygaard, P. Andersen, and E. Jansson. 1977. Fiber types and metabolic potentials of skeletal muscles in sedantary man and endurance runners. Annals of the New York Academy of Sciences 301:3–29.

Sato, K., and M. Mokha. 2009. Does Core Strength Training Influence Running Kinetics, Lower-Extremity Stability, and 5000-m Performance in Runners? The Journal of Strength & Conditioning Research 23.

Seeley, R., T. Stephens, and P. Tate. 2006. Anatomy and Physiology, 7th edition. McGraw Hill, New York, NY.

Simoneau, J. A., and C. Bouchard. 1995. Genetic determinism of fiber type proportion in human skeletal muscle. The FASEB Journal 9 :1091–1095.

Vollestad, N. K., and P. C. S. Blom. 1985. Effect of varying exercise intensity on glycogen depletion in human muscle fibres. Acta Physiologica Scandinavica 125:395–405.

Vollestad, N. K., I. Tabata, and J. I. Medbo. 1992. Glycogen breakdown in different human muscle fibre types during exhaustive exercise of short duration. Acta Physiologica Scandinavica 144:135–141.

Vollestad, N. K., O. D. D. Vaage, and L. Hermansen. 1984. Muscle glycogen depletion patterns in type I and subgroups of type II fibres during prolonged severe exercise in man. Acta Physiologica Scandinavica 122:433–441.

Wojtys, E. M., L. J. Huston, P. D. Taylor, and S. D. Bastian. 1996. Neuromuscular Adaptations in Isokinetic, Isotonic, and Agility Training Programs. The American Journal of Sports Medicine 24:187–192.

Zajac, F. E., and J. S. Faden. 1985. Relationship among recruitment order, axonal conduction velocity, and muscle-unit properties of type-identified motor units in cat plantaris muscle. Journal of Neurophysiology 53 :1303–1322.

Zierath, J. R., and J. a Hawley. 2004. Skeletal muscle fiber type: influence on contractile and metabolic properties. PLoS biology 2:e348.


How Much Do Genes Affect Your Athletic Potential? (Technical)

DNAGenes are heritable units, made of a sequence of deoxyribonucleic acid (DNA) contained in every cell of your body. They act as codes to produce all the proteins and determine all your characteristics from height, weight, color of skin and eyes to how good you are at memorizing stuff. Moving further in that line, genes determine your abilities as an athlete. Without going into the complexities of a complicated scientific explanation, you can just imagine those genes that code for the proteins building your calf and thigh muscles and the proteins in your blood that help carry oxygen, so that you  have lots of energy and don’t easily get tired while running fast. Precisely, all those are requirements for a good athlete.

Research has found that genetics (genetics is the study of genes) may determine 20-80% of an athlete’s performance. The twenty-first century witnessed a huge accomplishment in medical science – the completion of the Human Genome Project. It made available to us our entire genetic readout. Researchers have found that our abilities to perform strenuous physical activities is dependent on a number of our genes. We all have two copies of each gene, one inherited from our dad and the other from our mom. Let us imagine, a kid has a bad copy of the gene responsible for carrying oxygen in his blood. This will mean that he becomes a slower student in the physical education class compared to his fellow student who has both good copies of the same gene. Not only a particular gene, but also a specific variant of the gene is found more commonly in athletes, depending on what type of sports they perform – power or endurance type. Variants of a gene (also called alleles) refer to the different forms of a single gene that may be present in our body. Remember that genes are made of a sequence of DNA.

Now, this sequence readout may vary for the same gene. Depending on this difference of DNA sequence readout, a gene has one or more alleles. In 2003, a group of scientists from Australia demonstrated that ATCN-3 gene is closely related to athletic performance. ATCN-3 gene produces the protein α-actinin-3 expressed in fast-twitch muscle fibers and is responsible for generating force for high-velocity movement that is important for power sports. Two alleles of ACTN-3 have been found- R allele, producing the most active form of the protein and X allele, producing the less active form of the protein. The scientists found that male elite sprinters have a much higher frequency of RR (remember that we possess two copies of each gene) alleles of ATCN-3 gene than male elite endurance athletes and non-athletes. Elite endurance athletes predominantly possess the RX alleles. Studies by other research groups confirmed that there is extremely low to no frequency of XX alleles in most elite power athletes and this result is consistent in different racial groups accounted for in the studies.

Another potential ‘sports’ gene with distinct allelic drifts between power and endurance athletes is the ACE (Angiotensin converting enzyme) gene. ACE activates a hormone angiotensin that regulates constriction of your blood vessels, which in turn, controls the rate of blood flow through the circulatory system of your body.  Thus, ACE activity regulates blood pressure and has an effect on cardiac health. ACE also helps retain salt-water in your body that allows cells to stay healthy and metabolize better to produce lots of energy. The two most common variants of ACE are I and D. The I allele produces the enzyme with lower activity and the D allele produces the enzyme with increased activity. Scientists have found that endurance athletes like rowers and triathletes have a higher frequency of the I variant while the power athletes like elite swimmers and sprinters tend to possess the D allele. Many other genes related to respiratory capacity and cardiac health are being widely studied as associated with improved athletic capabilities. One such gene NRF1 is found more active in endurance athletes. And there are many more to add to this list that help determine an athlete’s potential or limitation.

So far, we have seen that apart from behavioral and environmental factors like rigorous training and exercise that are mostly accounted for contributing to athletic excellence, genetic predisposition also steers one’s chance towards being the star athlete. Some national team coaches even think it is beneficial to have genetic testing done on the candidates during selection of national team members. It will help them choose the handful who have the right genetic variant and thereby providing them with rigorous training, they can build a ‘superpower’ team. A Colorado-based genetics company called Altas Sports Genetics, that recently came into news, claims to offer inexpensive genetic tests to determine if a kid is predisposed towards the sports niche, and if at all, then to which type – endurance or power. This suggests parents can use this test to help them decide if their kid would excel on a baseball field or has great talents as a swimmer.

It is beneficial if the athletes have a basic knowledge of genes that relate to one’s athletic abilities. A detailed knowledge of those complex pathways by which these genes work is, however, not necessary. It is sufficient to know about the genetic variants and how they effect the physiology with respect to better athletic performance. It is, of course, not expected that every athlete has the right combinations. But, if they have the basic genetic knowledge that build up their ‘athletic’ physiology, it will be useful for them to customize their diet or training accordingly to promote better health and performance. Consider the example of the kid carrying one good copy of the gene regulating oxygen-carrying capacity of the blood. To supplement his genetic build-up, a diet rich in iron would make up for his inherent less oxygen-carrying capacity. He can also join specific yoga classes to help him be trained to be able to hold more oxygen volumes in his lungs.

It can become a matter of debate if the genetic information of the elite athletes would be made public. With genetic testing made widely available, it may happen that an athlete’s genetic information is made available on trading cards just like their height and weight. As a society, we tend to be curious of private lives of great athletes like Tiger Woods or David Beckham. The bigger a celebrity he is, the less privacy an athlete has in his life. Let alone the fact that the news overflows on their performance and abilities related to the sports; their personal lives, likes and dislikes, thoughts and emotions all get documented by the media. On top of this, the exposure of their genetic information to the public will leave them with almost no privacy. Alarmingly enough, the public exposure of their genetic information may even lead to viewing of the athlete’s successes to be generated not only from how well they perform based on years of perseverance but also from just their inherent traits.

However, it is not wise to consider one’s athletic abilities to be dependent on only the variations of a single or a couple of genes. The way our physiology is maintained in response to a network of genes and genetic pathways is far more complex than we can imagine. Gene expression is an entire field of study that investigates all those factors that help the expression of a gene to produce the functional protein. There are instances where you have the correct gene variant on your DNA strand, but it does not get expressed. It can be based on several factors like the effect of neighboring stretches of highly silent DNA regions (these regions on the DNA suppress the expression of their neighborhood genes) that eclipse the gene expression, presence of other silencer proteins inhibiting gene expression or absence of the helper proteins called transcription factors to induce gene expression. Thus, it seems less likely that all of the best athletes on this planet have the exact combination and proportionate expression of all the ‘superpower’ genes. Studies of the ATCN3 in a famous Olympic long jumper show that he has no copies of the R variant, but still he is the star. There are lots of environmental factors like nutrition, coaching, careful planning and a disciplined lifestyle that play a major part. You may have the right set of genes, but if you are a chain-smoker or a couch potato, you will ruin all your ‘inherent’ athletic potentials. Genes are, of course, important determinants of your predisposition in a particular field, but you must nurture yourself to reach your potential, otherwise, everything is just a waste. Whatever the genes are, you have to strive for excellence. The knowledge of genetics would help you to know more about yourself – what your body needs more of or it already has sufficiently. This will help your training and diet planned better to suit your needs. Have a positive mental attitude and keep working out harder – there is no reason why you can’t be a great athlete!


Riddhita Chakraborty, University of Utah, Department of Biology


Farrey, T. 2012. Genetic testing beckons. Retrieved from

Gaygay, G., B. Yu, B. Hambly, T. Boston, A. Hahn, D.S. Celermajer, and R.J. Trent. 1998. Elite endurance athletes and the ACE I allele – The role of gene in athletic performance. Human Genetics 103(1); 48-50.

Genetics role in athletic performance. 2012. Retrieved from

Greenbaum, D., and M. Gerstein. 2010. Exploring genetics for professional athletes. Retrieved from

Macur, J. 2008, November 28. Little ones get test of sports gene. Retrieved from

Meyerson, S., H. Hemingway, R. Budget, J. Martin, S. Humphries, and H. Montgomery. 1999. Human angiotensin I-converting enzyme gene and endurance performance. Journal of Applied Physiology 87(4); 1313-1316.

Nazarov, I.B., D.R. Woods, H.E. Montgomery, O.V. Shneider, V.I. Kazakov, N.V. Tomilin, and V.A. Rogozkin. 2001. The angiotensin converting enzyme gene I/D polymorphism in Russian athletes. European Journal of Human Genetics 9(10); 797-801.

O’Callaghan, T. 2010, May 12. Are elite athletes equipped with sports genes? Retrieved from

Ostrander, E.A., H.J. Huson, and G.K. Ostrander 2009. Genetics in athletic performance. Annual Review of Genomics and Human Genetics 10; 407-29.

Roth, S. M., S. Walsh, D. Liu, E.J. Metter, K. Ferrucci, and B.F. Hurley. 2008. The ATCN3 R577X nonsense allele is under-represented in elite-level strength athletes. European Journal of Human Genetics 16: 391-394.

Willams, J. 2008, December 21. Genetic testing for young athletes? . Retrieved from

Woods, D., M. Hickman, Y. Jamshidi, D. Brull, V. Vassiliou, A. Jones, S. Humphries, and H. Montgomery. 2001. Elite swimmers and the D allele of the ACE I/D polymorphism. Human Genetics 108(3); 230-232.

Yang, N., D. MacArthur, J. Gulbin, A. Hahn, A. Beggs, S. Easteal, and K. North. 2003. ACTN3 genotype is associated with human elite athletic performance. American Journal of Human Genetics. 73(3): 627-631.