Posted by Jackson Peos in Muscle Building
Estimated reading time: 7mins
Hubal et al. (2005), looked at differences in muscle size after 12 weeks of resistance training in 585 untrained adults. Subjects followed a program that only trained the biceps and triceps with linear progression over the entire duration of the program. Authors used MRIs to measure muscle cross-sectional area and found huge variability in muscle growth among subjects (from -2% to 59%), meaning the best responders increased muscle size by ~59% while the worst responders lost size! Even though total calorie and protein intake were not controlled in this study (and it is likely that some of the variations is due to differences in diet), it is still clear that an individual’s response to a given training program can be highly variable based upon genetic makeup.
The importance of myonuclear addition for muscle hypertrophy is still a very controversial concept. Although preliminary evidence does suggest that the number of available satellite cells (cells that repair old and form new muscle cells) is an important determinant of hypertrophic potential.
A study by Petrella et al. (2008) aimed to elucidate the concept that extreme muscle hypertrophy is facilitated by satellite cell rapid reproduction and the addition of new myonuclei to existing muscle fibres.
High responders, who experienced the greatest hypertrophic responses regardless of age and sex, also exhibited higher availability of satellite cells prior to training. Moreover, these individuals were found to be ‘more equipped’ to expand their satellite cell pool and create more myonuclei. High responders experienced hypertrophy increases up to 50% following 16 weeks of training, while individuals who exhibited lower satellite cells prior to training (low responders) saw no increase at all.
As shown by this study, genetics also play a very important role in myogenic potential and cell production. The authors summarized this premise concisely when they stated, “Expansion of the myonuclear domain may drive myonuclear addition by placing strain on existing nuclei to produce adequate gene products for the growing myofiber; however, the excessive increase in satellite cells seen among extreme responders suggests the induction of satellite cell proliferation is driven by factors beyond simply a demand for nuclear addition.”
Davidsen and colleagues conducted a study in 2011 examining fat-free mass increases following various post-workout supplement protocols. The authors aimed to determine the expression level of 21 miRNAs to determine whether variation in these miRNAs affected weightlifting-induced muscle gain variation. The authors took the top 15% (high responders) and bottom 15% (low responders) 15% and determined (by DEXA scan) that the high responders gained close to four times the lean mass than the low responders did.
One important thing to note is that several key microRNAs (molecules that regulate muscle protein synthesis) were identified and some were found to be correlated with the changes in lean body mass. Basically, this tells us those specific components of the genome are important determinants in one’s ability to build muscle. Currently, there is still insufficient literature to make informed assumptions upon this information, so it would be foolish to attempt to program training according to this premise but in my opinion, this sort of research is going to shape future practice remarkably.
Genes not only regulate muscle mass, but they also play a role in energy balance and nutrient partitioning, which in turn, regulate fat loss. A paper from Bouchard and colleagues overfed 12 pairs of twins by 1000 extra calories per day for 100 days. The authors concluded that there are substantial differences among individuals with respect to weight gain/loss and fat distribution.
Weight gain between subjects ranged from 9.5-29 lbs between twin pairs, and shockingly, some subjects experienced no increase in abdominal visceral fat while some subjects experienced 200% increases. Given such findings, the authors estimated that the heritability of metabolic factors involved in weight differences account for around 40% of the variation in weight gain and fat distribution!
An additional study by Schleinitz et al. (2014) identified that body fat distribution is also controlled by genetic factors independent of body mass index and overall obesity. The consensus from the study suggests that our body fat distribution is approximately 22-61% explained by our genetic heritability. It is important to mention that even though genes affect energy balance, this does not refute the fact that energy balance is the fundamental determinant of weight loss. There is no optimal macronutrient distribution when it comes to dealing with obesity. There is no perfect way of it, the best diet is the one you can stick to the most, adherence is key!
Humans are unique creatures, everybody knows that.
We also know that our genes are responsible for a big part of our individuality.
Genes not only influence how we build muscle but also how efficiently we store and lose fat (and from where).
Genetic factors really do control much more than we sometimes appreciate, but that should not prevent anyone from trying to create the best version of themselves.
In retrospect, we can now infer why some individuals respond better to different modalities of training programs and eating strategies. This is why experimentation with strategies is important, to allow you to find out which method works best for you and your genetics.