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Genes and Swimming Performance

Take Home Points on Genes and Swimming Performance

  1. Genetics likely contribute for swimming success, but are individualized to your ethnicity and distance specialty.
  2. Swimmers appear more reliant on ACE I/D, than the ACTN3 gene.

This is an excerpt from the March Swimming Science Research Review which is released on Friday March 15th. 

Make sure you pick your copy up today to enhance your swimming and evidence-based coaching.  


Genes and Swimming Performance

By now, everyone has heard of the 10,000 hour rule, a term coined from Dr.Ericsson's famous research and popularized by Gladwell. Unfortunately, this is mainstream view of genes and their involvement in sport (or any other area) is too simple. Dr. Tiago Barbosa broke down the guide to LTAD in swimmers, noting the role of genes for success. Genes play a role in athletic performance. The Sports Gene, a novel by David Epstein, discusses the influence of genes and performance.  Epstein's piece also questions the research by highlighting what is still unknown (see his interview on Sports Coach Radio). Genes play a role in sports, but the role for each person and for each sport is likely individual. 

Research on Genes and Swimming

Wang (2013) had two elite swimmer cohorts, comprising of Caucasian and East Asian subjects were analyzed. A total of 200 elite Caucasian swimmers (from Europe, American, and Russia) were sampled from 2005 – 2006 and categorized as short distance (less than 400 m; n=130) or long distance (less than 400 m; n=70). There were 116 male and 84 female Caucasian participants. East Asians comprised of short distance (less than 100 m; n=166) and middle distance (200 – 400 m; n=160). Females made up 130 subjects while the men made up 196 for the East Asian group. The East Asian group used Taiwanese and Japanese swimmers.

All the subjects underwent DNA sequencing and allele discriminatory testing.

Which Genes Improve Swimming Performance

The results suggested ACE I/D polymorphism is associated with elite swimmer status in both Caucasians and East Asians. The association is not seen in the longer-distance events in each group, but only in sprint middle distance swimmers in Caucasians and sprint distance swimmers in East Asians. ACTN3 p.R577X genotype was not significantly associated with swimmer status in these samples (unlike previous work in soccer players discussed in ACTN3 and Swimming Performance). In Caucasians ACE D allele was associated with elite status, versus the I allele in the East Asians. 

The varying allele association with success highlights some confusion, yet it may simply be that the sprinters are different than the middle distance swimmers or that different ethnicities have had different genetic alterations over the years. 

Also, the lack of ACTN3 association with success is surprising, as other sports demonstrate the ACTN3 is associated with greater power. This suggests swimming doesn’t rely on such power and perhaps relies more on biomechanics. Yet, there is contradictory evidence on ACTN3 and performance. Also, the classification of each swimmer's main activities is one limitation of this piece, since 50-m swimmers may have completely different genomes for success than 100-m swimmers (this applies to 200 and 400-m as well).

Practical Implication on Genes and Swimming Performance

Table of Contents March Swimming Science Research Review

  1. Perceived Effort Differs between Swimmers and Coaches | TRAINING
  2. Active Cool Down Decreases Lactate | RECOVERY
  3. Paddles Alter Swimming Force Production | PADDLES
  4. Individualization of Swim Suits | SWIM SUITS
  5. Force Asymmetry in Swimmers | BIOMECHANICS
  6. Swimming Minimally Increases Oxidative Stress | PHYSIOLOGY
  7. Snorkel Use Alters Breast Biomechanics | BIOMECHANICS
  8. Sex Differences in Swimmers | SWIMMING PERFORMANCE
  9. Genes and Performance | GENETICS
  10. Morning Practice Impairs Sleep | MORNING PRACTICE
  11. Different Pool Lengths Influence Performance | POOL LENGTH
  12. Salivary Proteins and Swimming Training | OVERTRAINING
  13. Peripheral Fatigue Limits Endurance | FATIGUE
  14. Bench Press Impairs Endurance Performance | TRAINING
  15. Fatigue and Thermal Stress | FATIGUE
  16. Comparing 400-m swim and 1500-m Run | SWIMMING PERFORMANCE
  17. Time-Trial Performance | TIME TRIALS
  18. Trends in Recreational Swimmers | LAP SWIMMING
  19. Practice Racing Breathing Strategies | BREATH TRAINING
  20. Oxygen Update in Swimmers | OXYGEN UPTAKE
  21. Decline in Performance with Age| PERFORMANCE
  22. Validating VO2max in nonexpert adults | MAXIMUM OXYGEN UPTAKE

Also, if you're interested in receiving updates on training and the abstract of the SSRR, don't forget to sign-up for our newsletter!
Email Address

Written by G. John Mullen who received his Doctorate in Physical at University of Southern California (USC) and is a certified strength and conditioning specialist (CSCS). At USC, he was a clinical research assistant performing research on adolescent diabetes, lung adaptations to swimming, and swimming biomechanics. G. John has been featured in Swimming World Magazine, Swimmer Magazine, and the International Society of Swim Coaches Journal. He is currently the owner of COR, providing Physical Therapy, Personal Training, and Swim Lessons to swimmers and athletes of all skills and ages. He is also the creator of the Swimmer's Shoulder SystemSwimming ScienceSwimming Science Research ReviewMobility System and the Swimming Troubleshooting System.
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Genotypes Influence Extensibility

Take Home Points:
  1. Genes influence extensiblity.
  2. A specific gene (or genes) may influence the extensibility at each joint.
  3. Altering this genotype may or may not be feasible, for improving your extensibility or your offsprings extensibility.
We have discussed stretching before on Swim Sci (Dryland Mistake: Stretching; Dryland Mistake: Stretching Part II; Dryland Mistake: Stretching Part III), but we haven't discussed the role of genes and mobility. It is well established genes play a role in all aspects of life, but since they are believed to be unmodifiable, they are often ignored. However, ignoring the issue never improves understanding the situation and how it can be influenced, in the immediate or far future. 

Kubo (2013) analyzed gene polymorphisms and their influence on tendon extensibility. This "study demonstrated that subjects with a CC genotype of the COL5A1 gene had more extensible tendon structures than those of subjects with other genotypes (combined TT and CT) for knee extensors, but not for plantar flexors. The results presented in this study need to be confirmed in a larger cohort of subjects Kubo 2013)".

Now, this research doesn't provide too many practical implications, as genes are rather static structures. However, this research does show the complexity of extensibility and how one gene (but likely many more) influence the extensibility at only one joint. However, a few questions still exist:

  • Does anything alter the expression of these genes? Without having a genetic test before and after altered extensibility, do we know if these genotypes are static?
  • The role of epigenetics, if you improved your extensibility would that increase the likelihood of your offspring having a CC genotype?
  1. Kubo K, Yata H, Tsunoda N. Effect of gene polymorphisms on the mechanical properties of human tendon structures. Springerplus. 2013 Jul 25;2:343. doi: 10.1186/2193-1801-2-343.
By Dr. G. John Mullen received his Doctorate in Physical Therapy from the University of Southern California and a Bachelor of Science of Health from Purdue University where he swam collegiately. He is the founder of Mullen Physical Therapy, the Center of Optimal Restoration, head strength coach at Santa Clara Swim Club, creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Weekly Round-up

  1. How sleep helps brain learn motor task.
  2. Fatigue shifts and scatters heart rate variability in elite endurance athletes. - by Dr. Schmitt
  3. The development of peripheral fatigue and short-term recovery during self-paced high-intensity exercise. - by Dr. Froyd
  4. Postural control and low back pain in elite athletes comparison of static balance in elite athletes with and without low back pain. - by Dr. Oyarzo
  5. Virtual swimming--breaststroke body movements facilitate vection. - by Dr. Seno
  6. Symmetry of support scull and vertical position stability in synchronized swimming. - by Dr. Winiarski
  7. Is bone tissue really affected by swimming? A systematic review.- by Gómez-Bruton
  8. Effect of gene polymorphisms on the mechanical properties of human tendon structures. - by Dr. Kubo
  9. Relation between efficiency and energy cost with coordination in aquatic locomotion. - by Dr. Figueiredo
  10. Is There a Minimum Intensity Threshold for Resistance Training-Induced Hypertrophic Adaptations? - by Brad Schoenfeld
  11. The Temporal Profile of Postactivation Potentiation is related to Strength Level. - by Dr. Seitz
  12. Athletes and novices are differently capable to recognize feint and non-feint actions. - by Dr. Güldenpenning 
  13. Effects of betaine on body composition, performance, and homocysteine thiolactone. - by Dr. Cholewa
  14. Fructose-Maltodextrin Ratio Governs Exogenous and Other CHO Oxidation and Performance. - by Dr. O'Brien
  15. Sports drink consumption and diet of children involved in organized sport. - by Dr. Tomlin
  16. Which exercises target the gluteal muscles while minimizing activation of the tensor fascia lata? Electromyographic assessment using fine-wire electrodes. - by Dr. Selkowitz
  17. Scapular Kinematics and Shoulder Elevation in a Traditional Push-Up. - by Dr. Suprak

Friday Interview: Kevin O'Connell Ph.D. Candidate Discusses Genes and Cramping

1. Please introduce yourself to the readers (how you started in the profession, education, credentials, experience, etc.).
Kevin O’Connell. I graduated from the University of Cape Town with a Bachelor of Science in Genetics and Development & Physiology in 2008. In 2009 I completed my honours degree in Exercise Science at the UCT/MRC Unit for Exercise Science and Sports Medicine. I registered for my MSc in Exercise Science in 2010 and was accepted as a PhD Candidate in 2012. My research focuses on collagen genes and their roles in the etiology of exercise-related traits.

2. You recently published an article on cramping, could you please explain what is

certain about genes?
The human genome is the complete set of human genetic information, stored as DNA sequences. The genome is made up of approximately 3.2 billion base pairs (letters). This DNA “alphabet” consists of only four base pairs; G, A, T and C (4 letters). Genes are made up of combinations of these base pairs, and can be hundreds or thousands of base pairs in length. The entire genome is packed into 23 pairs of chromosomes. One pair is inherited from your mother and the other from your father.

It is estimated that less than 2% of the human genome contains protein coding genes. To date approximately 21 000 protein coding genes have been identified which encode for >300 000 proteins. The remaining 98% of the human genome is referred to as non-coding DNA. Human DNA is approximately 99.9% identical. The remaining 0.1% is made up of single or multiple base pair sequence differences known as polymorphisms or variants. At each site an individual has one of two possible alleles (versions of the variant). A pair of alleles (one from each parent) is referred to as a genotype. These variants are of interest to researchers since they may alter gene expression and/or regulation.

3. Could you please explain your methods and why you believe genes play a role in cramping?
Cross-sectional studies have reported an association between a positive family history of exercise associated muscle cramps (EAMC) and increased risk of EAMC. A cross-sectional survey study highlighted family history of EAMC as a factor that is associated with a past history of EAMC in 1300 marathon runners (Manjra 2006). This association was later confirmed in a case-control study of 433 Ironman triathletes where the frequency of a positive family history of EAMC was significantly more common in triathletes with a past history of EAMC (36.6%) when compared to those with no history of EAMC (16.4%) (Shang 2011).

A number of hypotheses to explain the primary factors contributing to exercise associated muscle cramping (EAMC) have been proposed. These include the electrolyte depletion, dehydration and the more recent altered neuromuscular control hypotheses (Schwellnus 2009). The altered neuromuscular control hypothesis implicates a number of primary factors in the development of EAMC, including possible tissue damage (Schwellnus 2009).

In recent years, a number of genetic association studies have shown that there is a genetic predisposition to musculoskeletal soft tissue injuries ( including tendon and ligament injuries. Genes coding for the extracellular matrix component of the musculoskeletal soft tissue, including specific collagen genes, were associated in these studies (Posthumus 2009; Mokone 2006; September 2009). Since tissue damage and a familial predisposition may play a role in the etiology of EAMC, we hypothesised that variants within collagen genes that code for components of the musculoskeletal system increase susceptibility to EAMC.

Two hundred and sixty-eight Caucasian participants were recruited from the 2006 and 2007 226 km South African Ironman triathlon (n=211) or the 2009 and 2011 56 km Two Oceans ultra-marathon (n=57) for this study. One hundred and eighteen participants reported a history of EAMC within the last 12 months prior to the event (EAMC group), while 150 reported no history of a previous (lifelong) EAMC (NON group).

Participant genotypes were determined for variants within four collagen genes. The genotype frequency distributions, for each variant, were then compared between the EAMC group and NON group. Regression analysis was then used to determine if these genotypes contribute to the etiology of EAMC when accounting for other risk factors such as weight, height or injury.

4. What were the pertinent findings in your study?
The COL5A1 rs12722 (C/T) variant was associated with self-reported EAMC during the 12 months prior to participating in either the 2006 and 2007 South African Ironman triathlons or the 2009 and 2011 Two Oceans ultra-marathons. Specifically, the CC genotype was significantly over-represented in participants with no self-reported history of previous (lifelong) EAMC (CC genotype; 21.8%) when compared to participants that reported a past history of EAMC within 12 months prior to the event (CC genotype; 11.1%). Multivariate regression analysis also revealed the COL5A1 rs12722 TC and TT genotypes as positive contributors to risk of past history of EAMC. This is the first study to identify a genetic variant as a potential marker for a past history of EAMC. These results suggest that changes to type V collagen containing connective tissue may directly and/or indirectly modulate the risk of a past history of EAMC, however further investigation is required.

5. Do you think epigenetics play a role in collagen gene expression? If so, what do you think increases this gene expression?
Since we have identified a genetic component in the etiology of EAMC it is possible that epigenetics may also play a role. Epigenetics refers to heritable changes to the DNA sequence, such as DNA methylation patterns. These changes may, individually or in combination with gene variants, affect gene expression. Further research is required to test this hypothesis.

6. Why does the conventional wisdom persist that hydration levels cause exercise associated muscle cramps?

The belief that dehydration causes muscle cramps may be attributed to a number of factors. 1) This belief has been around for over 100 years, 2) textbooks used for educational purposes may not report the latest scientific findings, 3) evidence for the altered neuro-muscular control hypothesis is still being collected.

7. Despite your research and other similar findings, is it possible there's an indirect connection between hydration and EAMC?
The available evidence would suggest that an indirect connection between hydration or dehydration and EAMC does not exist.

8. Is there a practical way to find genetic makeup for those without access to genetic testing? Are there any recommended strategies for those who DO find they have the genetic predisposition to cramping?
Genetic testing for exercise-related traits, including EAMC, is premature. These traits are the consequence of multiple genetic and environmental factors which interact with one another. Although a number of gene variants and environmental factors have been identified the extent of their individual impact and how they interact still requires further research.

9. Any specific considerations for aquatic athletes (since that is different than ultra marathon, etc)
Athletes, including swimmers, should avoid inadequate conditioning. The result of inadequate conditioning is that athletes may then be under-prepared for competition intensity and/or duration. Over-exertion as a result of an increased relative exercise intensity and/or duration greatly increases risk of EAMC (Schwellnus 2009).

10. If someone is having a cramp, what can they do acutely?
The individual should stop exercising and rest. Assuming the individual does not suffer from any medical conditions that may be causing the cramping, passive stretching is the best form of treatment Miller 2010; Schwellnus 2008.

11. If someone is prone to cramps, what can they do chronically to prevent the occurrence?
Individuals prone to muscle cramping should avoid exercising in hot or humid conditions, exercise at lower intensities and for shorter durations, stretch affected muscles regularly and ensure that they have adequate nutritional intake 8. The individual may also consult a clinician about possible underlying medical conditions that may result in muscle cramping (Schwellnus 2008).

12. What mistakes still exist in professional athletes and rehabilitation clinics in regards to cramps?
Since a large number of people still follow the dehydration and electrolyte depletion hypotheses, over drinking and/or overuse of supplements to prevent EAMC can occur.

13. What research or projects are you currently working on or should we look from you in the future?
I am currently working on a review of genetic association studies investigating collagen genes and exercise-related traits which includes a hypothesis for how these variants may affect exercise-related traits. The paper should hopefully be published later this year.

  1. Manjra SI, Schwellnus MP, Noakes TD. Risk factors for exercise associated muscle cramping (EAMC) in marathon runners. Medicine and Science in Sports and Exercise. 1996;28:S167. 
  2. Shang G, Collins M, Schwellnus MP. Factors associated with a self-reported history of exercise-associated muscle cramps in ironman triathletes: a case-control study. Clinical Journal of Sport Medicine. 2011;21:204-210. 
  3. Schwellnus MP. Cause of exercise associated muscle cramps (EAMC)--altered neuromuscular control, dehydration or electrolyte depletion? British Journal of Sports Medicine. 2009;43:401-408. 
  4. Posthumus M, September AV, O'Cuinneagain D et al. The COL5A1 Gene Is Associated With Increased Risk of Anterior Cruciate Ligament Ruptures in Female Participants. Am J Sports Med. 4-8-2009;37:2234-2240. 
  5. Mokone GG, Schwellnus MP, Noakes TD et al. The COL5A1 gene and Achilles tendon pathology. Scand J Med Sci Sports. 2006;16:19-26. 
  6. September AV, Cook J, Handley CJ et al. Variants within the COL5A1 gene are associated with achilles tendinopathy in two populations. British Journal of Sports Medicine. 2009;43:357-365. 
  7. Miller KC, Stone MS, Huxel KC et al. Exercise-associated muscle cramps: causes, treatment, and prevention. Sports Health. 2010;2:279-283. 
  8. Schwellnus MP, Drew N, Collins M. Muscle cramping in athletes--risk factors, clinical assessment, and management. Clin Sports Med. 2008;27:183-18x.

ACTN3 and Swimming Performance

If you stay current with the scientific literature, you've undoubtedly noticed an increase in publications on genetics and performance, specifically ACTN3. 

ACTN3 and ACTN2 are major components of the skeletal muscle Z-disks. These components act as cross-linkers of actin thin filaments. ACTN3 is strictly found in fast twitch muscle fibers and is responsible for rapid contraction. ACTN3 may provide fast twitch fibers a higher capacity to absorb force at the Z-line during rapid contraction. 

Previous studies report no cases of Olympic sprint athletes had a ACTN3 deficiency. It seems clear ACTN3 is an important protein for sprint and power success. However, the effects of ACTN3 R577x polymorphism on human performance is not known. A recent study by Pimenta (2013) looked at the ACTN3 R577x polymorphism on human performance in elite soccer players. 

This study had these soccer players perform a group of agility and power exercises, in combination of receiving an extraction of their genomic DNA from the peripheral  blood samples. 

Individuals with RR presented with lower times in the 10m and greater jump tests than the XX genotype. The XX genotypes presented higher values for VO2max compared to the RR genotype.

The main finding is those with RR genotype have better power, while those with the XX genotype have higher VO2max.

Practical Implication
In swimming, those predisposed with a RR or RX genotype are likely more genetically predisposed to sprint events and those with the XX genotype are more suited for endurance events. However, swimming requires various distances, making it minimally beneficial for swimmers to determine their genetic makeup.

Moreover, as more studies surmount, it is necessary to remember genes are only part of a larger equation. 


  1. Pimenta EM, Coelho DB, Barros Coelho EJ, Cruz IR, Morandi RF, De Azambuja Pussieldi G, Santos Carvalho MR, Silami-Garcia E, De Paz Fernández JA. EFFECT OF GENE ACTN3 ON STRENGTH AND ENDURANCE IN SOCCER PLAYERS. J Strength Cond Res. 2013 Mar 27. [Epub ahead of print]
By Dr. G. John Mullen received his Doctorate in Physical Therapy from the University of Southern California and a Bachelor of Science of Health from Purdue University. He is the founder of the Center of Optimal Restoration, head strength coach at Santa Clara Swim Club, creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Black Sprint Swimmers

While watching the Olympics in the 100 m dash, anyone could tell black sprinters dominate the sport; this is especially noted in the 100-m distance.

This difference is evident and has been present for a while. However, controversy has surrounded this topic once again as Olympic Gold Medalist Michael Johnson releases his new book. In this book, Johnson discusses the benefits of slavery for athletes. The 44-year-old Texas native tells the Daily Mail "slavery has benefited descendants like me” and "I believe there is a superior athletic gene in us."

He goes on to refer to current research exploring "how much of a factor being descended from slaves contributes to athletic ability."

This is one athlete’s opinion, but he isn’t the only one with this idea. However, the thought of benefits don’t rectify the horrors of slavery.

As many know, this is a controversial subject. In the past, Jimmy the Greek, a sports commentator, was dismantled from his position due to comments on the African American athlete. This article strives to bring only research into the equation, specifically analyzing genes. Everyone has genetic advantages and disadvantages. If you believe in evolution, this is due to the slight genetic variations which occur constantly, Lamarckism. However, evolution does suggest we all came from the same being, making everyone related and the idea of racism and differences irrelevant. But, is the swimming community on the brink of the dominance of black sprint swimmers?

Gene Expression

Specific environments are believed to alter gene expression.

The geneticist, Rachael Irving, was quoted:

"There was not much oxygen on slave ships so they had to use whatever they had to survive."

It was survival of the fittest. A quick search of Dr. Irving returns an article from TrackLife, a Caribbean athletics magazine featuring her. Geneticist and exercise physiologist Claude Bouchard at Laval University in Quebec City has run numerous experiments comparing two populations, French-Canadian and West African students. Using long needles inserted into the thighs of test subjects, Bouchard's team extracted tiny sections of fibers, which look to the naked eye like pieces of raw meat. They were chemically treated to reveal metabolic differences, put on a glass slide, and slipped under a high-power microscope, where they appeared as a collage of tiny red and white crocodile scales. The West Africans, by a ratio of approximately two to one, had more of the larger fast-twitch fibers. The researchers concluded that the force generating capacity of type-II muscle fibers at high velocity, the speed and tempo of movements, and the capacity of an individual to adapt to exercise training are all genetically influenced. This is widely different from the great distance runners of East Africa (Kenya and Ethiopia), but could provide a benefit for black sprint swimmers.


The basic findings of that research showed 6 major physical differences: less body fat, short torsos, thinner hips, longer legs, thick thigh muscles, thinner calf muscles. The main physiological difference is a higher percentage of fast twitch fibers.

As Jimson points out, there are physiological differences, most notably the muscle fiber composition. Again, I feel this is a slight oversimplification, not on Jimson's part, but because I don't believe the science has really uncovered the secret of speed yet. But we're trying! In swimming, it is believed a long torso is beneficial, suggesting their anthropometrics may not be perfect for swimming, however it is difficult to argue the benefits the other characteristics. Moreover, these differences are not seen in every black person, therefore a combination of a long torso with longer legs is not unfathomable.

Different Genes

The finding of statistically similar mtDNA haplogroup distributions in Jamaican athletes and Jamaican controls suggests that elite Jamaican sprinters are derived from the same source population and there is neither population stratification nor isolation for sprint performance. The significant difference between African-American sprinters and African-American controls suggests that the maternal admixture may play a role in sprint performance (Deason 2012).

Given that ACTN3 XX genotype is negatively associated with elite sprint athlete status, the underlying low frequency in these populations eliminates the possibility of replicating this association in Jamaican and US African American sprinters. The finding of no excess in ACE DD or GG genotypes in elite sprint athletes relative to controls suggests that ACE genotype is not a determinant of elite sprint athlete status (Scott 2010).


In the sport of swimming, large efforts have been made to increase diversity. This is most notably the Make a Splash and Swim American campaigns. This result has increased diversity in this majority white sport.

With diversity slowly improving, we should expect to have African Americans begin to perform better at National and International competitions, most notably in sprint events. In my opinion, the biggest barrier to the minority population is availability. Luckily, the aforementioned campaigns suggest this as their site for improvement.

In swimming, the 50 free is the most powerful event and is likely where any athletic advantage would be found. However, will the increase in numbers result in more black sprint swimmers? Or, what are the largest contributors for success?

This history is already being written, as this past weekend 3 swimmers with African American (Cullen Jones, Anthony Ervin, Lia Neal) heritage competed at the Olympics.


Remember genes are not the only variable in the equation, but some feel sprinters are never created nor destroyed, suggesting the large role of genes. In swimming, motor control might be more important than other sports, suggesting genes might not contribute as much for black sprint swimmers, yet the sprint events might allow one to overcome the motor control component [personal belief]. The three main variables appear to be genes, training, and availability.


  1. Deason M, Scott R, Irwin L, Macaulay V, Fuku N, Tanaka M, Irving R, Charlton V, Morrison E, Austin K, Pitsiladis YP.Importance of mitochondrial haplotypes and maternal lineage in sprint performance among individuals of West African ancestry. Scand J Med Sci Sports. 2012 Apr;22(2):217-23. doi: 10.1111/j.1600-0838.2010.01289.x. Epub 2011 Mar 16.
  2. Scott RA, Irving R, Irwin L, Morrison E, Charlton V, Austin K, Tladi D, Deason ACTN3 and ACE genotypes in elite Jamaican and US sprinters. M, Headley SA, Kolkhorst FW, Yang N, North K, Pitsiladis YP. Med Sci Sports Exerc. 2010 Jan;42(1):107-12.
By G. John Mullen founder of the Center of Optimal Restoration, Swimming World Magazine Columnist, creator of the Swimmer's Shoulder System, and chief editor of the Swimming Science Research Review.

Training Swimming Genes

Genes and Performance Synchronization

The influence of genes on performance is a tantalizing subject with inappreciable complexity. This dense subject is impossible to breakdown. In fact, it is so complex even the top scientist from around the world have only began to scratch the surface in understanding the genetic influence in athletics. Some are oblivious to the idea of genetic influence, while others are convinced genes are all which matter. Unfortunately, the volume of genes influencing athletic performance is plentiful, with tons of small influences, too difficult to track at the moment.

Malcolm Gladwell suggested in his critically acclaimed book "Blink" that 10,000 hours of deliberate practice will make one an expert. This simplistic view only tells a fraction of the story, as anyone in the swimming community knows countless stories of athletes who have spent a lifetime practicing, only to stay mediocre, while others have risen to the top in no time. One plausible explanation for this difference are genes. In fact, research has suggested 28% of variance in darts performance was due to 15 years of practice, which begs the question where do the other 72% lie? You may scuff this idea, considering darts an inappreciable comparison, but swimming and darts both rely on many factors.

Sports performance is a highly complex subject. To reiterate, sports performance is the result of hundreds or possibly thousands of variables. Practice, coaching, time-spent learning are obvious variables. This is why elite athletes can come from all walks of life and countries where opportunity exist. Practice is an influential variable to offset potential differences in innate ability, but is it large enough to make anyone world class...I don't think so, but this isn't suggesting training is irrelevant.

Unfortunately, much of the media differentiates genes and practice. Early evidence supports the notion that genes and practice are additive variables. Many view genes as a static entity, but genes are an open environment, increasing and decreasing expression depending on variables (practice, nutrition, etc.). For example, one could be myostatin deficient, but if they are starved of all nutrients they will never reach their maximal muscle potential. This is because the myostatin deficient genes weren't fully expressed due to the lack of nutrients. This must be acknowledged and appreciated to begin understanding the variability and complexity of genetic influence. This article will discuss the influence of training on genes.
10,000 Hour Theory
Whether you are a follower of the 10,000 hour training philosophy, all must accept genes impact training. It is clear some people adapt to training faster than others, or they are able to rapidly acquire skills. Everyone grew up playing outside, remembers a kid who was able to learn everything rapidly. Whether it was trying to learn basketball, soccer or breath holding, these outliers were able to concur the task before any of their peers. Certain activities come faster to some than others. To determine the results of genes and training, one must apply the exact training to a specific group and track the adaptations. Each year swim coaches this case study approach to their team. They provide nearly the same workout to everyone on the team and watch how they respond. If training was the only variable, then each swimmer would theorectically improve the same amount each year. As coaches know, this is far from the case. Also, how hard someone works can correlate with success, but sometimes it doesn't. This open system is highly dependent on many variables, one which is genes.

There are no swimming studies looking at the cumulative effect of the exact training program, but Bouchard 2011 applied a five month training stimulus to 470 untrained adults. Bouchard et al. used VO2max improvements as their resultant of training. These researchers found on average, an improvement of 300-500 ml/min with the subjects. However, 7% of the participants only improved 100 ml/min, whereas 4% improved 950 ml/min. The greatest improvement in VO2max was 1000 ml/min, with the least improvement with 100 ml/min. This 10-fold difference is astonishing for only five months of training. Imagine how the differences after 20 years of swim training! The athlete with a large adaptations in training is likely to be an elite distance swimmer and the athlete with a 100 ml/min improvement is likely watching from the stands.
This study is beneficial , but one flaw is not looking at the starting point of the athletes. The researchers tried to decrease the importance of this variable by using all "untrained" adults, but if Lance Armstrong didn't exercise for 6 months would he be classified as "untrained"...
To illustrate, those with a high VO2max, may have a limited room for improvement. This will decrease their potential to improve their VO2max. For example, if one of these untrained athletes had a starting VO2max of 900 ml/min. After training lets say they improve their VO2max to 1000 ml/min. The net change of 100 ml/min would be viewed as a low responder. Imagine another athlete with a starting VO2max of 100 ml/min. After training, they may improve up to 900 ml/min, a net improvement of 800 ml/min, making them a high responder, but an overall lower VO2max than the low responder discussed. This vast difference in training is likely the resultant of various genes.

Potential Outliers
Everyone has heard of elite swimmers who have succeeded with less than 10,000 hours of training. For example, lets use Phelps (MP) at the age of 14 making the Olympics. We will say MP started swimming at age five and swan two hours a day for 10 years. I understand he didn't swim only two hours a day in his early teens, but he also didn't swim two hours a day, everyday a week when he was five, so we'll call it even. If he swam this volume he would have only swam 7,300 hours total (this assumes he swam everyday for 9 years). This is 1/4 less than the 10,000 hours to become an expert in the field.

The second point is that there is no good evidence at all to suggest that 10,000 hours is required for expert performance. The study that is always cited is a violin study, which found that expert violinists had accumulated an AVERAGE of 10,000 hours by the time they went to music school, whereas those who were merely good had done 8,000 hours. Two problems. First, you can't infer cause from this kind of retrospective study. Who is to say that the talented, genetically gifted violinists didn't train more BECAUSE they had more talent from the age of 8? Perhaps their innate ability was the catalyst to get them more practice (mom sends them for lessons, and they enjoy it). And secondly, the study showed absolutely no indication of ranges or variance. So we don't know whether there are some people who became experts with less training, and nor do we know whether some failed despite doing their 10,000 hours, because the author did not show that data. I hope I don't have to emphasize that if either of these people exist, then the theory is wrong.

On the other end of the spectrum, everyone is more familiar with athletes who put in 10,000 hours but fail. For example, specific Master's swimmers have been swimming for the past 40 years and have yet to reach elite levels and sometimes are far from even average swimmers. It is unfortunate 10,000 didn't get them to elite status, but even more upsetting that 20,000 or 30,000 hours will leave them short of athletic success.

In sport, countless studies show that elite athletes get to the top within 6,000 hours of starting their sport. These are likely the high responders to exercise. Imagine if Talent Identification followed athletes during their first couple thousand hours of training and determined if they improved enough to be a high responder...crazy.

The bottom line is that a theory of deliberate practice gives us one important message - if you want to succeed, practice. Coaches around the world breathe a sigh of relief, you're not redundant. But this is so obvious, I guess the reminder is always good though.

However, the application of this theory is potentially false and damaging. Some don't want to reward those with superior genes or success, to provide a "participation trophy" society. This is fine to help kids improve participation, but if we want to find the next Olympic swimmer, then being naive to genes will hinder athletic success.

Not only this, but it could be extremely damaging. If you take it literally, and you buy into a 10,000 hour concept, then you'll likely start training a child at the age of about 10, because you need them to become world-class in their early-20s. All good and well, except the evidence shows quite clearly that the earlier you start intensive training, the LESS likely you are to succeed. And so there are all kinds of implications for how we manage child's sport participation. Every coach knows the swimmer who saw success as an age-group swimmer, then was pushed by their parents to succeed only to become a second rate swimmer. This process must be patient, as rushing it can lead to distaste with sport or all exercise.

Dr. Ross from the Sports Scientist said it best 
"training is nothing more than the realization of genetic potential". Without both, you will not become an Olympic champion (in a competitive sport, that is). Training will improve everyone, and so everyone should be encouraged to train. But genetic factors determine where we start, how we respond to training (trainability), how much training we can tolerate before burnout or injury (because let's face it, chess players rarely get injuries that force 6-week layoffs, like stress fractures), and finally, where the "performance ceiling" exists."

By Dr. G. John Mullen, DPT, CSCS. He is the founder of the Center of Optimal Restoration and head strength coach at Santa Clara Swim Club.