As per my previous paper on genetics, I've found hundreds of abstracts showing the variance of genetic potential between different races and individual athletes:
The frequency of the α-actinin-3–deficient genotype (577XX) varies from 25% in Asian populations to <1% in an African Bantu population; the frequency in Europeans is ∼18%. This raises the possibility that ACTN3 genotype confers differential fitness in humans, under certain environmental conditions. The force-generating capacity of type 2 muscle fibers at high velocity, the speed and tempo of movements, and
the capacity of the individual to adapt to exercise training are all strongly genetically influenced (Rankinen et al. 2002).
Cluster analysis tests the importance of myogenic gene expression during myofiber hypertrophy in humans.
Bamman MM, Petrella JK, Kim JS, Mayhew DL, Cross JM.
Source
Department of Physiology and Biophysics, Medical Scientist Training Program, The University of Alabama at Birmingham, and Core Muscle Research Laboratory, GRECC/11G, Veterans Affairs Medical Center, AL 35294-0001, USA.
[email protected]
Abstract
We applied K-means cluster analysis to test the hypothesis that muscle-specific factors known to modulate protein synthesis and satellite cell activity would be differentially expressed during progressive resistance training (PRT, 16 wk) in 66 human subjects experiencing extreme, modest, and failed myofiber hypertrophy. Muscle mRNA expression of IGF-I isoform Ea (IGF-IEa), mechanogrowth factor (MGF, IGF-IEc), myogenin, and MyoD were assessed in muscle biopsies collected at baseline (T1) and 24 h after the first (T2) and last (T3) loading bouts from previously untrained subjects clustered as extreme responders (Xtr, n=17), modest responders (Mod, n=32), and nonresponders (Non, n=17) based on mean myofiber hypertrophy. Myofiber growth averaged 2,475 microm2 in Xtr, 1,111 microm2 in Mod, and -16 microm2 in Non. Main training effects revealed increases in all transcripts (46-83%, P<0.005). For the entire cohort, IGF-IEa, MGF, and myogenin mRNAs were upregulated by T2 (P<0.05), while MyoD did not increase significantly until T3 (P<0.001). Within clusters, MGF and myogenin upregulation was robust in Xtr (126% and 65%) and Mod (73% and 41%) vs. no changes in Non. While significant in all clusters by T3, IGF-IEa increased most in Xtr (105%) and least in Non (44%). Although MyoD expression increased overall, no changes within clusters were detected.
We reveal for the first time that MGF and myogenin transcripts are differentially expressed in subjects experiencing varying degrees of PRT-mediated myofiber hypertrophy. The data strongly suggest the load-mediated induction of these genes may initiate important actions necessary to promote myofiber growth during PRT, while the role of MyoD is less clear.
http://www.ncbi.nlm.nih.gov/pubmed/17395765
Association of interleukin-15 protein and interleukin-15 receptor genetic variation with resistance exercise training responses
Steven E. Riechman1, G. Balasekaran1, Stephen M. Roth2, and Robert E. Ferrell1
+ Author Affiliations
1Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania 15260; and 2Department of Kinesiology, University of Maryland, College Park, Maryland 20742
Address for reprint requests and other correspondence: S. E. Riechman, A300 Crabtree Hall, University of Pittsburgh, Pittsburgh, PA 15260 (E-mail:
[email protected])
Submitted 6 May 2004. Accepted 16 July 2004.
Abstract
Interleukin-15 (IL-15) is an anabolic cytokine that is produced in skeletal muscle and directly affects muscle anabolism in animal and in vitro models. The contribution of IL-15 variability in muscle responses to 10 wk of resistance exercise training in young men and women was examined by measuring acute and chronic changes in IL-15 protein in plasma and characterizing genetic variation in the IL-15 receptor-α gene (IL15RA). Participants trained 3 days a week at 75% of one repetition maximum, performing three sets (6–10 repetitions) of 13 resistance exercises. Plasma IL-15 protein was significantly increased (P < 0.05) immediately after acute resistance exercise but did not change with training and was not associated with variability in muscle responses with training. A single nucleotide polymorphism in exon 7 of IL15RA was strongly associated with muscle hypertrophy and accounted for 7.1% of the variation in regression modeling. A polymorphism in exon 4 was also independently associated with muscle hypertrophy and accounted for an additional 3.5% of the variation in hypertrophy. These results suggest that IL-15 is an important mediator of muscle mass response to resistance exercise training in humans and that genetic variation in IL15RA accounts for a significant proportion of the variability in this response.
http://jap.physiology.org/content/97/6/2214.short
ACTN3 genotype is associated with human elite athletic performance.
Yang N, MacArthur DG, Gulbin JP, Hahn AG, Beggs AH, Easteal S, North K.
Source
Institute for Neuromuscular Research, Children's Hospital at Westmead, Sydney, Australia.
Abstract
There is increasing evidence for strong genetic influences on athletic performance and for an evolutionary "trade-off" between performance traits for speed and endurance activities. We have recently demonstrated that the skeletal-muscle actin-binding protein alpha-actinin-3 is absent in 18% of healthy white individuals because of homozygosity for a common stop-codon polymorphism in the ACTN3 gene, R577X. alpha-Actinin-3 is specifically expressed in fast-twitch myofibers responsible for generating force at high velocity. The absence of a disease phenotype secondary to alpha-actinin-3 deficiency is likely due to compensation by the homologous protein, alpha-actinin-2. However, the high degree of evolutionary conservation of ACTN3 suggests function(s) independent of ACTN2. Here, we demonstrate highly significant associations between ACTN3 genotype and athletic performance. Both male and female elite sprint athletes have significantly higher frequencies of the 577R allele than do controls. This suggests that the presence of alpha-actinin-3 has a beneficial effect on the function of skeletal muscle in generating forceful contractions at high velocity, and provides an evolutionary advantage because of increased sprint performance. There is also a genotype effect in female sprint and endurance athletes, with higher than expected numbers of 577RX heterozygotes among sprint athletes and lower than expected numbers among endurance athletes. The lack of a similar effect in males suggests that the ACTN3 genotype affects athletic performance differently in males and females. The differential effects in sprint and endurance athletes suggests that the R577X polymorphism may have been maintained in the human population by balancing natural selection.
http://www.ncbi.nlm.nih.gov/pubmed/12879365
