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Just published a new article, What is the Meaning of "Genetics" for Bodybuilding?
Author: Type-IIx
I. Introduction
Genes are sequences of DNA that transcribe proteins – that comprise all of our tissues and cells, including blood – and form the genetic code for what ultimately makes up the matter that makes us human, forming us into being. Genes exist on the 26 chromosome pairs that we inherit from our parents in equal measure. This genetic code of a human sets the range or domain, the capacity for achievement. Genetic capacity is a vector quantity, it has both magnitude and speed. Those who are endowed with great bodybuilding capacity have a larger pool or reserve to fill (i.e., LBM) than the average or sub-average person (i.e., magnitude), as well as having a more rapid rate of progress (i.e., speed).
Bodybuilding, the competitive endeavor of attaining an outstanding lean, muscular physique, requires optimizing the aspects of training, nutrition, and physique-enhancing drug (PED) planning and implementation – the nurture, or environmental factors – in a manner that fulfills the genetic capacity or endowment of the bodybuilder – the nature, or inherited factors, on very long time-frames. Typically, decadeslong patterns of progressive training across resistance and aerobic endurance modes is a necessary but not sufficient condition to maximize one's genetic capacity. One must, also, be well nourished, intentionally counting energy and macronutrients (e.g., carbohydrate to support intensive muscular work, protein to synthesize new muscle tissue). The bodybuilder must constantly optimize balancing efficacy/tolerability tradeoffs inherent to use the use of hormonal agents that have, by their nature, pluripotent action (affecting virtually all systems and tissues). Finally, the bodybuilder must vigilantly, obsessively, strive for marginal gains in an effort to achieve his full capacity: to step on stage and strain the very limits of physiological and biological possibility to their apex.
I.1. Purpose and Scope
This article is not intended as a complete reference to all facets of genetic capacity for bodybuilding. That, besides presumptuous, would simply be impossible. Rather, it's intended as a high-level review of significant known factors involved in maximizing one's genetic capacity for bodybuilding.
II. Optimization
II.1. Training
Bodybuilders must have large quantities of muscle mass, so resistance training is paramount. There is broad inter-individual heterogeneity in response (ΔLBM) to resistance training such that increased skeletal muscle is not a consistent effect in the general population as an adaptation to any given resistance training program. [1]. In fact, skeletal muscle is actually lost in many cases despite strength consistent strength increases. [1]. This means that there is no one-size-fits all approach – individualization of the training is crucial.
Heritability estimates for muscle mass or cross-sectional area range between 0.20 and 0.95, with several studies reporting heritabilities at about 0.85 (3). [2]. Candidate genes include the ACTN3 gene that exemplifies functional involvement in the functional unit of the muscle (the sarcomere). [2]. Other candidate genes include MYLK (myosin light-chain kinase), IGF-related genes (e.g., IGF1, IGFBP3), MSTN, and the inflammatory factors and neurotrophic factors (e.g., CCR2). [2].
ACE, ACTN3, and PPARGC1A genes are associated with optimal training volumes (barbell lifts) in weightlifters. [3].
The ACE ID (heterozygous) and DD genotypes were significantly more adaptable to lower workloads (requiring lower macrocycle load volumes). The II genotype is associated with low adaptation to training volumes. [3].
The PPARGC1A SS genotype was associated with elite strength/power: athletes with the SS genotype maintained a high level of sports achievements with small amounts of training in the meso- and macro- structure of training (fast-trained phenotype). Conversely, GS was OK (intermediate), and GG required almost triple the volume load vs. PPARGC1A/SS (slowly-trained or 'hard-gainer' phenotype). [3].
The ACTN3 (Alpha-actinin-3) RX genotype was associated with high adaptation to optimal training volumes (e.g., 18,200 lifts in the macrocycle). The XX genotype required more than triple the volume load (sucks), RR was OK (21,480 lifts). [4].
Given high heritability coefficients (~ 85%) of muscularity, it is likely that genetic capacity is under the control of key genes including those described above, affecting both the magnitude or absolute LBM one can hold and the speed of tissue accrual.
II.2. Physique-Enhancing Drug Tolerability/Efficacy
Compound selection, setting the initial dose, and titration, all depend on balancing efficacy/tolerability tradeoffs, with respect to all anabolic, partitioning, and fat loss agents used by bodybuilders. The Push Factors vs. Pull Factors depend largely on the bodybuilder's capacity – his genes. Optimal dosing is neither minimally-effective nor maximally-tolerable. It is, optimal, in the Goldilocks Zone, "neither too hot nor too cold, but just right."
With respect to AAS, within the AR gene (AR), the length of the polymorphic polyglutamine CAG repeat is a marker for AR sensitivity (capacity to respond to T as a ligand), with longer CAG repeats indicative of lower AR sensitivity. [5]. Lower doses, then, are inherently more tolerable because there's less circulating toxic androgen to reach other tissues at concentrations that cause detrimental effects. Likewise, the Esterase gene (PDE7B), of which there are 2 variants, the rs7774640 A allele confers a 56% greater bioavailability (AUC) of parent steroid vs. the G allele. [6].
With respect to rhGH, the GH receptor (GHR) gene determines GH response, with exon 3 deletion (d3d3/homozygous) a marker of male-specific exceptional longevity associated with increased GH sensitivity and taller stature. [7].
II.3. Nutrition
For the sake of brevity, it is due just passing mention that insulin sensitivity, obesogenic phenotypes, gut insensitivities, are too under genetic control. Nobody would argue with a type 1 diabetic that he was born insulin resistant due to his genetics. The human physiology is wildly varied, thanks to random "bits" of adenine, guanine, cytosine, and thymine and the miracle of genetics.
Conclusion
Bodybuilding's intrigue is rooted in its meteoric pursuit to push the human limits of physiology right to their very limits, blending art, science, and good old-fashion grit.
The important take-away for the reader is this:
No person can possibly ascertain the breadth or depth their capacity ("genetic potential," "genetics," "talent,") until well after diminishing returns have set in after years of optimal effort, and may only after optimizing all facets (training, nutrition, drugs) simultaneously even begin to appreciate the basic contours of the maximal speed at which he can maximize his genetic capacity.
Of course, genetic capacity, in those who possess it, carry a responsibility, too – as the adage says, "there is nothing sadder than wasted talent."
VI. References
[1] Carpinelli, Ralph. (2017). Interindividual Heterogeneity of Adaptations to Resistance Training.
[2] Thomis, M. A., & Aerssens, J. (2012). Genetic variation in human muscle strength—opportunities for therapeutic interventions? Current Opinion in Pharmacology, 12(3), 355–362. doi:10.1016/j.coph.2012.03.003
[3] Aksenov, M.O., Ilyin, A.B. Training process design in weightlifting sports customized to genetic predispositions. Teoriya i praktika fiz. kultury, 21.07.2018.
[4] Yang, MacArthur, Gulbin, Hahn, Beggs, et al. ACTN3 genotype is associated with elite athletic performance. American Journal of Human Genetics 73 627-631. 2003.
[5] Medland, S. E., Duffy, D. L., Spurdle, A. B., Wright, M. J., Geffen, G. M., Montgomery, G. W., & Martin, N. G. (2005). Opposite Effects of Androgen Receptor CAG Repeat Length on Increased Risk of Left-Handedness in Males and Females. Behavior Genetics, 35(6), 735–744.
[6] Ekström, L., Schulze, J. J., Guillemette, C., Belanger, A., & Rane, A. (2011). Bioavailability of testosterone enanthate dependent on genetic variation in the phosphodiesterase 7B but not on the uridine 5′-diphospho-glucuronosyltransferase (UGT2B17) gene. Pharmacogenetics and Genomics, 21(6), 325–332. doi:10.1097/fpc.0b013e328344c5c6
[7] Bianchi, A., Giampietro, A., Tartaglione, L., Chiloiro, S., Gentilella, R., Bima, C., … De Marinis, L. (2019). Short and long-term responsiveness to low dose GH in adult Growth Hormone Deficiency (GHD): role of GH receptor (GHR) polymorphism. Journal of Neuroendocrinology, e12692. doi:10.1111/jne.12692
Author: Type-IIx
I. Introduction
Genes are sequences of DNA that transcribe proteins – that comprise all of our tissues and cells, including blood – and form the genetic code for what ultimately makes up the matter that makes us human, forming us into being. Genes exist on the 26 chromosome pairs that we inherit from our parents in equal measure. This genetic code of a human sets the range or domain, the capacity for achievement. Genetic capacity is a vector quantity, it has both magnitude and speed. Those who are endowed with great bodybuilding capacity have a larger pool or reserve to fill (i.e., LBM) than the average or sub-average person (i.e., magnitude), as well as having a more rapid rate of progress (i.e., speed).
Bodybuilding, the competitive endeavor of attaining an outstanding lean, muscular physique, requires optimizing the aspects of training, nutrition, and physique-enhancing drug (PED) planning and implementation – the nurture, or environmental factors – in a manner that fulfills the genetic capacity or endowment of the bodybuilder – the nature, or inherited factors, on very long time-frames. Typically, decadeslong patterns of progressive training across resistance and aerobic endurance modes is a necessary but not sufficient condition to maximize one's genetic capacity. One must, also, be well nourished, intentionally counting energy and macronutrients (e.g., carbohydrate to support intensive muscular work, protein to synthesize new muscle tissue). The bodybuilder must constantly optimize balancing efficacy/tolerability tradeoffs inherent to use the use of hormonal agents that have, by their nature, pluripotent action (affecting virtually all systems and tissues). Finally, the bodybuilder must vigilantly, obsessively, strive for marginal gains in an effort to achieve his full capacity: to step on stage and strain the very limits of physiological and biological possibility to their apex.
I.1. Purpose and Scope
This article is not intended as a complete reference to all facets of genetic capacity for bodybuilding. That, besides presumptuous, would simply be impossible. Rather, it's intended as a high-level review of significant known factors involved in maximizing one's genetic capacity for bodybuilding.
II. Optimization
II.1. Training
Bodybuilders must have large quantities of muscle mass, so resistance training is paramount. There is broad inter-individual heterogeneity in response (ΔLBM) to resistance training such that increased skeletal muscle is not a consistent effect in the general population as an adaptation to any given resistance training program. [1]. In fact, skeletal muscle is actually lost in many cases despite strength consistent strength increases. [1]. This means that there is no one-size-fits all approach – individualization of the training is crucial.
Heritability estimates for muscle mass or cross-sectional area range between 0.20 and 0.95, with several studies reporting heritabilities at about 0.85 (3). [2]. Candidate genes include the ACTN3 gene that exemplifies functional involvement in the functional unit of the muscle (the sarcomere). [2]. Other candidate genes include MYLK (myosin light-chain kinase), IGF-related genes (e.g., IGF1, IGFBP3), MSTN, and the inflammatory factors and neurotrophic factors (e.g., CCR2). [2].
ACE, ACTN3, and PPARGC1A genes are associated with optimal training volumes (barbell lifts) in weightlifters. [3].
The ACE ID (heterozygous) and DD genotypes were significantly more adaptable to lower workloads (requiring lower macrocycle load volumes). The II genotype is associated with low adaptation to training volumes. [3].
The PPARGC1A SS genotype was associated with elite strength/power: athletes with the SS genotype maintained a high level of sports achievements with small amounts of training in the meso- and macro- structure of training (fast-trained phenotype). Conversely, GS was OK (intermediate), and GG required almost triple the volume load vs. PPARGC1A/SS (slowly-trained or 'hard-gainer' phenotype). [3].
The ACTN3 (Alpha-actinin-3) RX genotype was associated with high adaptation to optimal training volumes (e.g., 18,200 lifts in the macrocycle). The XX genotype required more than triple the volume load (sucks), RR was OK (21,480 lifts). [4].
Given high heritability coefficients (~ 85%) of muscularity, it is likely that genetic capacity is under the control of key genes including those described above, affecting both the magnitude or absolute LBM one can hold and the speed of tissue accrual.
II.2. Physique-Enhancing Drug Tolerability/Efficacy
Compound selection, setting the initial dose, and titration, all depend on balancing efficacy/tolerability tradeoffs, with respect to all anabolic, partitioning, and fat loss agents used by bodybuilders. The Push Factors vs. Pull Factors depend largely on the bodybuilder's capacity – his genes. Optimal dosing is neither minimally-effective nor maximally-tolerable. It is, optimal, in the Goldilocks Zone, "neither too hot nor too cold, but just right."
With respect to AAS, within the AR gene (AR), the length of the polymorphic polyglutamine CAG repeat is a marker for AR sensitivity (capacity to respond to T as a ligand), with longer CAG repeats indicative of lower AR sensitivity. [5]. Lower doses, then, are inherently more tolerable because there's less circulating toxic androgen to reach other tissues at concentrations that cause detrimental effects. Likewise, the Esterase gene (PDE7B), of which there are 2 variants, the rs7774640 A allele confers a 56% greater bioavailability (AUC) of parent steroid vs. the G allele. [6].
With respect to rhGH, the GH receptor (GHR) gene determines GH response, with exon 3 deletion (d3d3/homozygous) a marker of male-specific exceptional longevity associated with increased GH sensitivity and taller stature. [7].
II.3. Nutrition
For the sake of brevity, it is due just passing mention that insulin sensitivity, obesogenic phenotypes, gut insensitivities, are too under genetic control. Nobody would argue with a type 1 diabetic that he was born insulin resistant due to his genetics. The human physiology is wildly varied, thanks to random "bits" of adenine, guanine, cytosine, and thymine and the miracle of genetics.
Conclusion
Bodybuilding's intrigue is rooted in its meteoric pursuit to push the human limits of physiology right to their very limits, blending art, science, and good old-fashion grit.
The important take-away for the reader is this:
No person can possibly ascertain the breadth or depth their capacity ("genetic potential," "genetics," "talent,") until well after diminishing returns have set in after years of optimal effort, and may only after optimizing all facets (training, nutrition, drugs) simultaneously even begin to appreciate the basic contours of the maximal speed at which he can maximize his genetic capacity.
Of course, genetic capacity, in those who possess it, carry a responsibility, too – as the adage says, "there is nothing sadder than wasted talent."
VI. References
[1] Carpinelli, Ralph. (2017). Interindividual Heterogeneity of Adaptations to Resistance Training.
[2] Thomis, M. A., & Aerssens, J. (2012). Genetic variation in human muscle strength—opportunities for therapeutic interventions? Current Opinion in Pharmacology, 12(3), 355–362. doi:10.1016/j.coph.2012.03.003
[3] Aksenov, M.O., Ilyin, A.B. Training process design in weightlifting sports customized to genetic predispositions. Teoriya i praktika fiz. kultury, 21.07.2018.
[4] Yang, MacArthur, Gulbin, Hahn, Beggs, et al. ACTN3 genotype is associated with elite athletic performance. American Journal of Human Genetics 73 627-631. 2003.
[5] Medland, S. E., Duffy, D. L., Spurdle, A. B., Wright, M. J., Geffen, G. M., Montgomery, G. W., & Martin, N. G. (2005). Opposite Effects of Androgen Receptor CAG Repeat Length on Increased Risk of Left-Handedness in Males and Females. Behavior Genetics, 35(6), 735–744.
[6] Ekström, L., Schulze, J. J., Guillemette, C., Belanger, A., & Rane, A. (2011). Bioavailability of testosterone enanthate dependent on genetic variation in the phosphodiesterase 7B but not on the uridine 5′-diphospho-glucuronosyltransferase (UGT2B17) gene. Pharmacogenetics and Genomics, 21(6), 325–332. doi:10.1097/fpc.0b013e328344c5c6
[7] Bianchi, A., Giampietro, A., Tartaglione, L., Chiloiro, S., Gentilella, R., Bima, C., … De Marinis, L. (2019). Short and long-term responsiveness to low dose GH in adult Growth Hormone Deficiency (GHD): role of GH receptor (GHR) polymorphism. Journal of Neuroendocrinology, e12692. doi:10.1111/jne.12692
