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The truth about bodybuilding genetics

Die Wahrheit über Bodybuilding Genetik

How the mutants do it

Andy Bolton, who set a world record in the deadlift, was able to move 225 kilos in squats and 270 kilos in deadlifts when he tried these two exercises for the very first time.

Former Mr. Olympia Dorian Yates bench pressed 140 kilos on his first attempt as a teenager.

The owner of the Metroflex Gym Brian Dobson tells a story about his first meeting with the then powerlifter and later Mr. Olympia Ronnie Coleman. He describes Ronnie's enormous thighs with veins protruding through the elastane - even though Ronnie had never used anabolic steroids at the time.

Arnold Schwarzenegger looked more muscular after one year of bodybuilding training than most people do after 10 years of training.

It is very obvious that some individuals respond much better to training than others. But what makes the elite respond so much better than us "ordinary" people?

Genetics: The cold, hard truth

This is something you probably don't want to hear, but your progress depends largely on your genetic predispositions.

Recent research has shown that some individuals respond very well to strength training, while others barely respond, and still others don't respond at all. You read that right. Some people show no visible results. Scientists have created the term "non-responders" for these people.

The scientific studies

A groundbreaking study conducted by Hubal with 585 male and female subjects showed that 12 weeks of progressive dynamic training resulted in a shockingly wide range of responses.

The worst responders to the training lost 2% of their muscle cross-sectional area and built no strength at all. The best responders were able to increase their muscle cross-sectional area by 59% and increase their 1RM strength by 250%. You should keep in mind that all subjects followed the exact same training program.

The Hubal study is not the only study to show these types of results. Petrella, in a study of 66 subjects, showed that 16 weeks of progressive dynamic training produced no measurable hypertrophy in 26% of subjects. Wow, it must suck to be one of them.

The question that arises against this background is what mechanisms explain this. Let's look at the current study situation.

How genetics influence muscle growth

There is strong evidence that the results you see in the gym are heavily dependent on the efficiency of satellite cell-mediated myonuclear addition. In simple terms, your muscles will not grow until the satellite cells surrounding your muscle fibers donate their nuclei to your muscles so that your muscles can produce more genetic material to signal the cells to grow.

Petrella showed that the difference between people who responded excellently to strength training compared to people who did not respond to strength training was mainly in the area of saddle cell activation. People who respond excellently to strength training have more satellite cells surrounding their muscles and an amazing ability to expand their satellite cell pool via training.

In this study, people who responded excellently to strength training had an average of 21 satellite cells per 100 muscle fibers at the beginning of the study and this number had increased to 30 satellite cells per 100 muscle fibers after 16 weeks of training. This was accompanied by a 54% increase in average muscle cross-sectional area. The people who did not respond to strength training had 10 satellite cells per 100 muscle fibers at the beginning of the study and this number did not change over the course of the study, which also applied to their muscle mass.

Another study conducted by Bamman, which involved exactly the same experiment, showed that out of 66 subjects, the 17 subjects who responded best to the training achieved a 58% increase in muscle cross-sectional area, while the 32 subjects who were in the middle range were able to increase their muscle cross-sectional area by 28% and the 17 subjects in the lower range were not able to increase their muscle cross-sectional area at all.

The following could also be observed:

  • An upregulation of mechanogrowth factor (MGF) by 126% in the top 17 subjects and by 0% in the 17 worst responders.
  • An upregulation of myogenin by 65% in the top 17 subjects and by 0% in the 17 worst responders.
  • An upregulation of IGF-IEa by 105% in the top 17 subjects and only 44% in the 17 worst responders.

Research conducted by Timmons showed that there were several highly expressed miRNAs in the 20% of subjects who were the worst responders in a prolonged resistance training intervention study.

Research conducted by Dennis showed that individuals with high expression of key hypertrophies had a clear adaptive advantage over "normal" individuals. Individuals with lower initial expression of key hypertrophies showed lower adaptations to strength training despite the fact that training increased their gene expression in response to training.

The bottom line

Some people have hit the genetic jackpot, while others have drawn a genetic blank. Genetically, anything that reduces the ability of myofibers to increase their number of nuclei in response to a mechanical load will reduce both hypertrophy and strength potential.

This ranges from the number of signaling molecules, the sensitivity of the cells to these signals, the availability of satellite cells and the expansion of the satellite cell pool, to miRNA regulation. Of course, nutrition and an optimal training program also play a role in hypertrophy, and certain genotypes may also be associated with hypertrophy.

Genetics and body fat

Genes can affect fat storage and fat loss by influencing energy intake, energy expenditure and/or nutrient partitioning. Scientists have created the term "obesogenic environment" to describe the way in which lifestyle changes over the last century have revealed our underlying genetic risk factors for excessive fat storage.

Natural selection has favored those who possess genes associated with a thrifty metabolism, which would allow survival during times of food scarcity. However, as much of the world's population today has adopted a modern lifestyle characterized by physical inactivity and excessive caloric intake, these same genes now contribute to poor health and overweight/obesity.

The scientific research

Bouchard took 12 pairs of twins and had them eat 1000 kcal above their maintenance calorie allowance for 84 out of 100 days, totaling 84,000 excess kcal. The subjects maintained a sedentary lifestyle during this time. The average weight gain was 17.86 pounds, but the range of weight gain ranged from 9.48 to 29.32 pounds!

Even when all subjects followed the same diet, the most metabolically "cursed" subjects gained more than three times the amount of weight compared to the most metabolically "blessed" subject, storing 100% of excess calories in their body tissues (compared to only 40% for the subject on the other end of the spectrum) and increasing their visceral abdominal fat by 200% (compared to 0% for the subject on the other end of the spectrum).

Similar variances were observed by Bouchard in twins who consumed a constant amount of energy while exercising regularly.

Perusse showed that genetic predisposition is responsible for 42% of subcutaneous fat and 56% of visceral abdominal fat. This means that individual genetics strongly influence where you store fat and some individuals have an alarming predisposition to store fat in their abdominal region.

Bouchard and Tremblay estimated that 40% of the variability in resting metabolic rate, the thermic effect of food and the energy cost of low to moderate intensity exercise is genetically determined. They also reported that habitual physical activity is strongly influenced by genetic predisposition.

Loos and Bouchard suggest that overweight and obesity have a genetic cause and that sequence variations in the adrenergic receptors, uncoupling proteins, peroxisome proliferator activated receptor and leptin receptor genes are of particular relevance.

O'Rahilly and Farooqi added that the insulin VNTR and IGF-1 SNPs are also associated with obesity, and Cotsapas showed 16 different loci that influence body mass index (BMI), all of which are associated with extreme obesity. Rankinen identified hundreds of possible gene candidates that could promote the development of obesity.

Fawcett and Barroso showed that fat mass and the obesity-associated gene (FTO) is the first universally accepted locus to be clearly linked to obesity. FTO deficiency protects against obesity and elevated levels promote obesity, which is most likely due to increased appetite and reduced energy expenditure.

Tercjak adds that FTO can also influence insulin resistance and suggests that over 100 genes influence overweight and obesity. Herrerra and Lindgren list 23 genes associated with obesity and suggest that hereditary factors are responsible for 40 to 70% of BMI!

Faith found evidence for a genetic influence on calorie intake. Similar conclusions were drawn by Choquette, who studied the eating behavior of 836 subjects and found six genetic links to increased calorie and macronutrient consumption. These included the adiponectin gene.

What does all this mean? It means that some individuals have a genetic predisposition to obesity and fat storage in the abdominal area.

But are some people born to be excellent athletes, while others are born to warm the bench? Let's find out.

Genetics and athleticism

Although we still have a lot to learn about genetics when it comes to human performance, we know that many different genes can influence performance.

The scientific studies

Bray et al (2009) reviewed the current knowledge of human genes that influence performance and concluded that 214 autosomal genes and loci, as well as 18 mitochondrial genes, appear to influence fitness and performance.

The best known performance-enhancing gene is ACTN3, also known as alpha-actin-3.

There are two alpha-actin proteins: ACTN2 and ACTN3. Alpha-actins are structural proteins of the Z-lines in muscle fibers and while ACTN2 is found in all fiber types, ACTN3 is preferentially found in type IIb muscle fibers. These fibers are involved in force production during high acceleration, which is the reason ACTN3 is associated with force production.

About 18% of all people - or over a billion people worldwide - cannot produce ACTN3 at all and their bodies generate more ACTN2 to compensate. These people cannot perform explosive movements as fast as their alpha-actin-3 producing counterparts and, as has been shown, elite sprinters almost never suffer from alpha-actin-3 deficiency (Yang).

The ACE gene - also known as the antiotensin converting enzyme - is also associated with human performance. Increased ACE D allele frequency is associated with power and sprint athletes, while increased allele frequency of ACE I is associated with endurance athletes (Nazarov).

Cauci showed that variations in the VNTR IL-1RN genes are associated with better athleticism. This gene influences the interleukin family of cytokines and promotes the inflammatory response and repair process after exercise. Reichman's work supports this research, as they found that the interleukin-15 protein and its receptor can be linked to increased muscle hypertrophy.

Numerous other genes, including the myostatin gene, also show a potential to improve athletic performance. However, there is no conclusive evidence yet, or we simply don't have a good enough understanding of the whole puzzle.

Don't panic - you're not doomed!

Although the research reviewed in this article can seem quite daunting, I have something to say about this.

First of all, we all have genetic predisposition issues that we need to work around. Some of us have a predisposition to excessive fat gain, some of us are lean but have stubborn fat deposits, some of us have problems building muscle and some of us are muscular but have a weak muscle group. Some of us have all these problems at once and no one has perfect genetics!

My list of genetic curses is a mile long, but I've still managed to build a pretty respectable body and achieve reasonably impressive strength levels. Secondly, the protocols used in this research involved no experimentation, no adaptations and no autoregulatory training. We all need to adjust the variables and find our individual optimal training methodology.

Some people respond best to variety, some best to volume, some best to intensity, some best to high training frequency and others best to high training density. You need to find the best stimuli for your body that will evolve over time.

Third, I have talked to my colleagues about this topic and we agree on the following: we have never trained anyone who did not look better after a few months of training than when they started - assuming, of course, that they followed the program. All of these individuals have lost fat and improved their shape.

While some individuals have a much easier time developing an impressive body than others, I have yet to see an individual who has trained intelligently achieve any results.

So even if you are a so-called "hardgainer" and don't respond well to training and nutrition, you can and will see results if you are consistent and if you keep experimenting. Of course, the rate and extent of adaptations will be heavily influenced by your genetics, but sound and sensible training methods will always be responsible for a large part of the training effects.

The lesson is this: Your genetic makeup makes a difference, but smart training, smart nutrition and smart supplementation can help you maximize what your parents passed on to you.

References

  1. Hubal MJ, Gordish-Dressman H, Thompson PD, Price TB, Hoffman EP, Angelopoulos TJ, Gordon PM, Moyna NM, Pescatello LS, Visich PS, Zoeller RF, Seip RL, Clarkson PM. Variability in muscle size and strength gain after unilateral resistance training. Med Sci Sports Exerc 37: 964-972, 2005.
  2. Petrella JK, Kim JS, Mayhew DL, Cross JM, Bamman MM. Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol 104: 1736-1742, 2008.
  3. Bamman MM, Petrella JK, Kim JS, Mayhew DL, Cross JM. Cluster analysis tests the importance of myogenic gene expression during myofiber hypertrophy in humans. J Appl Physiol 102: 2232-2239, 2007.
  4. Timmons JA. Variability in training-induced skeletal muscle adaptation. J Appl Physiol [Epub ahead of print], 2010.
  5. Dennis RA, Zhu H, Kortebein PM, Bush HM, Harvey JF, Sullivan DH, Peterson CA. Muscle expression of genes associated with inflammation, growth, and remodeling is strongly correlated in older adults with resistance training outcomes. Physiol Genomics 38(2):169-75, 2009.
  6. Bouchard C, Tremblay A, Despres JP, Nadeau A, Lupien PJ, Theriault G, Dussault J, Moorjani S, Pinault S, Fournier G. The response to long-term overfeeding in identical twins. N Engl J Med. 322(21):1477-1482, 1990.
  7. Bouchard C, Tremblay A, Despres JP, Theriault G, Nadeau A, Lupien PJ, Moorjani S, Prudhomme D, Fournier G. The response to exercise with constant energy intake in identical twins. Obes Res 2:400-410, 1994.
  8. Perusse L, Despres JP, Lemieux S, Rice T, Rao DC, Bouchard C. Familial aggregation of abdominal visceral fat level: results from the Quebec family study. Metabolism 45:378-382, 1996.
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  10. Loos RJ and Bouchard C. Obesity - is it a genetic disorder? J Intern Med254(5) 401-25, 2003.
  11. Cotsapas C, Speliotes EK, Hatoum IJ, et al: Common body mass index-associated variants confer risk of extreme obesity. Hum Mol Genet 18:3502-3507, 2009.
  12. Rankinen T, Zuberi A, Chagnon YC, Weisnagel SJ, Argyropoulos G, Walts B, Perusse L, Bouchard C. The human obesity gene map: the 2005 update. Obesity (Silver Spring) 14(4):529-644, 2006.
  13. Fawcett KA, Barroso I. The genetics of obesity: FTO leads the way. Trends Genet. pp. 266-274, 2010.
  14. Tercjak M, Luczynski W, Wawrusiewicz-Kurylonek N, Bossowski A. The role of FTO gene polymorphism in the pathogenesis of obesity. Pediatr Endocrinol Diabetes Metab 16(2) 109-13, 2010.
  15. Herrera B and Lindgren C. The genetics of obesity. Curr Diab Rep 10:498-505, 2010.
  16. Faith MS, Rha SS, Neale MC, Allison DB. Evidence for genetic influences on human energy intake: results from a twin study using measured observations.Behav Genet 29:145-54, 1999.
  17. Choquette AC, Lemieux S, Tremblay A, Chagnon YC, Bouchard C, Vohl MC, Perusse L. Evidence of a quantitative trait locus for energy and macronutrient intakes on chromosome 3q27.3: the Quebec Family Study. Am J Clin Nutr 88(4): 1142-8, 2008.
  18. Bray MS, Hagberg JM, Perusse L, Rankinen T, Roth SM, Wolfarth B, Bouchard C. The human gene map for performance and health-related fitness phenotypes: the 2006-2007 update. Med Sci Sports Exerc 41: 35- 73, 2009.
  19. Cauci S, Santolo M, Ryckmann KK, Williams SM, Banfi F. Variable number of tandem repeat polymorphisms of the interleukin-1 receptor antagonist gene IL-1RN: a novel association with the athlete status. BMC Med Genet 11(29) 2010.
  20. O'Rahilly S., Farooqi I.S. Genetics of obesity. Philos. Trans. R. Soc. Lond. B Biol. Sci. 361:1095-1105, 2006.
  21. Riechman SE, Balasekaran G, Roth SM, Ferrell RE. Association of interleukin-15 protein and interleukin-15 receptor genetic variation with resistance exercise training responses. J Appl Physiol 97: 2214-2219, 2004.
  22. Yang N, MacArthur DG, Gulbin JP, Hahn AG, Beggs AH, Easteal S, North K. ACTN3 genotype is associated with human elite athletic performance.Am J Hum Genet 73: 627-631, 2003.
  23. Nazarov IB, Woods DR, Montgomery HE, Shneider OV, Kazakov VI, Tomilin NV, Rogozkin VA (2001) The angiotensin converting enzyme I/D polymorphism in Russian athletes. Eur J Hum Genet 9:797-801, 2001.

Source: https://www.t-nation.com/training/truth-about-bodybuilding-genetics

By Bret Contreras

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