This is by Bret Contreras -- frankly one of the most knowledgeable and authoritative writers I know of on the science of this.
for understanding this stuff, I highly recommend reading these articles that explain the whole process of hypertrophy. it's a lot more than just testosterone:
1. http://suppversity.blogspot.com/2011...ilding_18.html
2. http://suppversity.blogspot.com/2011...ilding_25.html
3. http://suppversity.blogspot.com/2012...-building.html
4. http://suppversity.blogspot.com/2012...ilding_02.html
5. http://suppversity.blogspot.com/2012...ilding_08.html
6. http://suppversity.blogspot.com/2012...ilding_15.html
7. http://suppversity.blogspot.com/2012...-thoughts.html
choice quotes:
A landmark study by Hubal used 585 male and female human subjects and showed that twelve weeks of progressive dynamic exercise resulted in a shockingly wide range of responses.
The worst responders lost 2% of their muscle cross-sectional area and didn't gain any strength whatsoever. The best responders increased muscle cross-sectional area by 59% and increased their 1RM strength by 250%. Keep in mind these individuals were subjected to the exact same training protocol.
The worst responders lost 2% of their muscle cross-sectional area and didn't gain any strength whatsoever. The best responders increased muscle cross-sectional area by 59% and increased their 1RM strength by 250%. Keep in mind these individuals were subjected to the exact same training protocol.
The Hubal study isn't the only study showing these types of results. Petrella showed that 16 weeks of progressive dynamic exercise involving 66 human subjects failed to yield any measurable hypertrophy in 26% of subjects. Wow, sucks to be them!
...
Petralla showed that the difference between excellent responders in comparison to average and non-responders in strength training was mostly due to satellite cell activation. Excellent responders have more satellite cells that surround their muscle fibers, as well as a remarkable ability to expand their satellite cell pool via training.
In this study, excellent responders averaged 21 satellite cells per 100 fibers at baseline, which rose to 30 satellite cells per 100 fibers by week sixteen. This was accompanied by a 54% increase in mean fiber area. The non-responders averaged 10 satellite cells per 100 myofibers at baseline, which did not change post-training, nor did their hypertrophy.
...
Petralla showed that the difference between excellent responders in comparison to average and non-responders in strength training was mostly due to satellite cell activation. Excellent responders have more satellite cells that surround their muscle fibers, as well as a remarkable ability to expand their satellite cell pool via training.
In this study, excellent responders averaged 21 satellite cells per 100 fibers at baseline, which rose to 30 satellite cells per 100 fibers by week sixteen. This was accompanied by a 54% increase in mean fiber area. The non-responders averaged 10 satellite cells per 100 myofibers at baseline, which did not change post-training, nor did their hypertrophy.
A different article by Bamman using the same researchers involving the exact same experiment showed that out of 66 subjects, the top 17 responders experienced a 58% gain in cross-sectional area, the middle 32 responders gained 28% cross-sectional area, and the bottom 17 responders didn't gain in cross-sectional area. In addition:
• Mechanogrowth factor (MGF) upregulated 126% in the top 17 responders and 0% in the bottom 17 responders.
• Myogenin upregulated 65% in the top 17 responders and 0% in the bottom 17 responders.
• IGF-IEa upregulated 105% in the top 17 responders and only 44% in the bottom 17 responders.
• Mechanogrowth factor (MGF) upregulated 126% in the top 17 responders and 0% in the bottom 17 responders.
• Myogenin upregulated 65% in the top 17 responders and 0% in the bottom 17 responders.
• IGF-IEa upregulated 105% in the top 17 responders and only 44% in the bottom 17 responders.
Research by Timmons indicates that there are several highly expressed miRNAs that are selectivity regulated in subjects representing the lowest 20% of responders in a longitudinal resistance training intervention study.
Research by Dennis showed that individuals who have high expression of key hypertrophy genes have a distinct adaptive advantage over normal individuals. Individuals with lower baseline expression of key hypertrophy genes showed less adaptations to strength training, despite the fact that training did increase their gene expression in response to exercise.
Bouchard took twelve pairs of twins and subjected them to 84 days over a 100-day period of overfeeding by 1,000 calories per day, for a total of 84,000 excess calories. Subjects maintained a sedentary lifestyle during this time. The average weight gain was 17.86 pounds, but the range went from 9.48 pounds to 29.32 pounds!
Even though each subject adhered to the same feeding schedule, the most metabolically cursed individual gained more than triple the weight than the most metabolically blessed individual, stored 100% of excess calories in his tissues (compared to only 40% tissue storage for the most-blessed individual), and increased abdominal visceral fat by 200% (compared to 0% in the case of the most-blessed individual).
Even though each subject adhered to the same feeding schedule, the most metabolically cursed individual gained more than triple the weight than the most metabolically blessed individual, stored 100% of excess calories in his tissues (compared to only 40% tissue storage for the most-blessed individual), and increased abdominal visceral fat by 200% (compared to 0% in the case of the most-blessed individual).
...many different genes can affect performance.
Bray et al. (2009) mapped out the current knowledge of human genes that affect performance as of 2007 and concluded that 214 autosomal genes and loci as well as 18 mitochondrial genes appear to influence fitness and performance.
The most popular 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 expressed in all fiber types, ACTN3 is preferentially expressed in type IIb fiber types. These fibers are involved in force production at high velocities, which is why ACTN3 is associated with powerful force production.
Approximately 18% of individuals, or one billion people worldwide, are completely deficient in ACTN3 and their bodies create more ACTN2 to make up for the absence. These individuals just can't explode as quickly as their alpha-actin-3-containing counterparts, as elite sprinters are almost never alpha-actin-3 deficient (Yang).
The ACE gene, also known as the antiotensin converting enzyme, has also been implicated in human performance. An increase in the frequency of the ACE D allele is associated with power and sprint athletes, while an increased frequency of the ACE I allele is associated with endurance athletes (Nazarov).
Bray et al. (2009) mapped out the current knowledge of human genes that affect performance as of 2007 and concluded that 214 autosomal genes and loci as well as 18 mitochondrial genes appear to influence fitness and performance.
The most popular 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 expressed in all fiber types, ACTN3 is preferentially expressed in type IIb fiber types. These fibers are involved in force production at high velocities, which is why ACTN3 is associated with powerful force production.
Approximately 18% of individuals, or one billion people worldwide, are completely deficient in ACTN3 and their bodies create more ACTN2 to make up for the absence. These individuals just can't explode as quickly as their alpha-actin-3-containing counterparts, as elite sprinters are almost never alpha-actin-3 deficient (Yang).
The ACE gene, also known as the antiotensin converting enzyme, has also been implicated in human performance. An increase in the frequency of the ACE D allele is associated with power and sprint athletes, while an increased frequency of the ACE I allele is associated with endurance athletes (Nazarov).
"Genetically-speaking, anything that negatively impacts the ability of the myofibers to increase their number of myonuclei in response to mechanical loading will reduce hypertrophy and strength potential. This ranges from the number of signaling molecules, to the cell's sensitivity to the signals, to satellite cell availability, to satellite cell pool expansion, to miRNA regulation. Nutrition and optimal programming play a role in hypertrophy of course, and certain genotypes may be associated with hypertrophy too."
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