Seeing as Aaron was so friendly about it....
It was a poster presentation. I can't remember where from.
I've got some other bits and pieces....
Re: Flex Wheeler
To whom it may concern:
I am writing this letter per the request of Flex Wheeler.
I would first like to briefly provide you with some background information regarding BALCO Laboratories. BALCO has been working with elite Olympic and professional athletes for over fifteen years. BALCO has provided testing and consultation for over 250 NFL players including the entire 1998 Super Bowl Champion Denver Broncos team and the entire Miami Dolphins team. BALCO works with professional athletes in many sports including teenis (Michael Chang, Jim Courier, etc.), hockey, bodybuilding (10 of the 16 1998 Mr. Olympia contestants), track and field, soccer and basketball (Seattle SuperSonics).
BALCO Laboratories has been testing and monitoring Flex on a routine basis during the last year. We have performed tests including blood chemistry (SMAC), complete blood count (CBC), PSA, anabolic hormone levels, genotyping as well as comprehensive testing for nutritional elements. Flex's test results have been compared to twenty-four other professional bodybuilders and overall he has one of the healthiest profiles. Basically, Flex is in excellent health and has demonstrated the discipline necessary to maintain a peak level of conditioning.
Flex was a participant in a study we recently conducted in collaboration with the Department of Human Genetics at the University of Pittsburgh involving 62 men who made unusually large gains in muscle mass in response to strength training (extreme responders). Flex was one of only nine extreme responders that had the very rare "myostatin mutation." Myostatin is the gene that "limits muscle growth." Specifically, Flex had the rarest form of myostatin mutation at the "exon 2" position on the gene. This simply means Flex has a much larger number of muscle fibers compared to the other subjects or the normal population. We believe that these are the very first myostatin mutation findings in humans and the results of this landmark study have already been submitted for publication. Flex was also found to have a very unusual type of the IGF-1 gene. In fact, Flex was the only participant in the study that did not have a "match." All of the other extreme responders had at least three other subjects with a matching IGF-1 gene. Based upon Flex's very unique genetic profile, we plan to expeditiously publish a scientific paper that reveals his complete genotype in specific detail. The publication of his remarkable genetic data should generate an enormous amount of media exposure.
Hope this information will be helpful and please call if I can be of assistance.
Sincerely,
/s/ Victor Conte
Victor Conte
President
BALCO Laboratories, Inc.
1520 Gilbreth Road • Burlingame, CA 94010 • 1-800-777-7122 • FAX (650) 687-6576
MATERIALS AND METHODS
Sequencing of selected regions of the myostatin gene and genotyping
of common variants were carried out in a comparison sample of
96 randomly selected Caucasian and 96 African American subjects
from the general population. An additional 72 individuals were
screened for a common exon 2 variant. One hundred fifty-three
subjects, including 127 men (32 African American, 91 Caucasian,
and 4 Asian) and 26 women (9 African American, 16 Caucasian, and
1 Asian), were categorized by the magnitude of increases in muscle
mass they experienced from strength training. The subjects consisted
of world-class bodybuilders (ranked in the top 100 worldwide)
(N 5 18; 5 were ranked in the top 10), competitive bodybuilders not
ranked in the top 100 (N 5 25), elite power lifters (N 5 7), university
football players (N 5 9), previously untrained subjects who had their
quadricep muscle volume measured by magnetic resonance imaging
before and after 9 weeks of heavy resistance strength training of the
knee extensors (N 5 33), and nonathletes, who were questioned
about their ability to increase their muscle mass in response to
intense and prolonged strength training (N 5 61). A rating of 5 was
given to those who were world-class bodybuilders and to those who
increased their quadriceps muscle mass by .400 cm3 after only 9
weeks of strength training, whereas a rating of 0 was given to those
who experienced no noticeable increase in muscle mass after vigorous
strength training for at least 6 months. Eighteen subjects received
a rating of 5, and 13 subjects received a rating of 0. The
ratings of the remaining subjects fell somewhere between these two
extremes. Subjects who were rated as either 4 or 5 were classified as
extreme responders (N 5 62) and were compared to those who were
rated as either 0 or 1 and were classified as nonresponders (N 5 48).
Subjects were also grouped and compared by race. Information on
muscle mass changes with strength training from the remaining
subjects was obtained through either estimates of fat-free mass
assessed by dual-energy X-ray absorptiometry or hydrodensitometry
or in the case of competitive bodybuilders, power lifters, football
players, and nonathletes, through questionnaire data on prior success
in bodybuilding competition and/or reported changes in muscle
mass with strength training. Informed consent was obtained from all
subjects under protocols approved by the Institutional Review
Boards of the University of Maryland and the University of Pittsburgh.
Laboratory methods. Genomic DNA was prepared from EDTA
anticoagulated whole blood or from cheek swabs by standard methods
(Miller et al., 1988). DNA amplification primers for each exon and
the 59-flanking region of the human myostatin gene were designed
based on the cDNA sequence of human myostatin (GenBank Accession
No. AF019627) and the genomic organization of the bovine
myostatin gene (Grobet et al., 1997).
it is interesting to note that three of the
African American nonresponders were homozygous for
the less common (Arg) allele at the exon 2 K153R site,
while none of the responders were homozygous for this
allele. Three of the five mutations causing the doublemuscle
phenotype in cattle occur in exon 2 and are
recessive, but two are chain termination mutations
and one is a deletion, expected to produce a nonfunctional
myostatin protein (Grobet et al., 1998). Whether
variation in the myostatin gene influences muscle phenotypes
other than the muscle mass increase in response
to strength training requires further exploration.
1: J Appl Physiol. 2007 Mar 8;
Activin RIIB and Follistatin Haplotype Associations with Muscle Mass and Strength in Humans.
Walsh S, Metter EJ, Ferrucci L, Roth SM.
PURPOSE: Genetic variation in myostatin, a negative regulator of skeletal muscle, in cattle has shown remarkable influence on skeletal muscle resulting in a double-muscled phenotype in certain breeds; however, DNA sequence variation within this gene in humans has not been consistently associated with skeletal muscle mass or strength. Follistatin and Activin RIIB (ACVR2B) are two myostatin-related genes involved in the regulation/signaling of myostatin. We sought to identify associations between genetic variation and haplotype structure in both follistatin and ACVR2B with skeletal muscle related phenotypes. METHODS: Three hundred and fifteen males and 278 females aged 19-90 years from the Baltimore Longitudinal Study of Aging were genotyped to determine respective haplotype groupings based on HapMap data. Whole-body soft tissue composition was measured by dual-energy X-ray absorptiometry. Quadriceps peak torque (strength) was measured using an isokinetic dynamometer. RESULTS: Women carriers of ACVR2B haplotype group 1 exhibited significantly less quadriceps muscle strength (shortening phase) than women homozygous for haplotype group 2 (109.2 +/- 1.9 vs 118.6 +/- 4.1 N.m, 30 degrees /sec, respectively, p = 0.036). No significant association was observed in men. Male carriers of follistatin haplotype group 3 exhibited significantly less total leg FFM than non-carriers (16.6 +/- 0.3 vs 17.5 +/- 0.2 kg, respectively, p = 0.012). No significant associations between these haplotype groups were observed in women. CONCLUSION: These results indicate that haplotype structure at the ACVR2B and follistatin loci may contribute to inter-individual variation in skeletal muscle mass and strength, though these data indicate sex-specific relationships. Key words: genetics, skeletal muscle, myostatin, sex.
PMID: 17347381 [PubMed - as supplied by publisher]
Interview with the doctor from the study
It was a poster presentation. I can't remember where from.
I've got some other bits and pieces....
Re: Flex Wheeler
To whom it may concern:
I am writing this letter per the request of Flex Wheeler.
I would first like to briefly provide you with some background information regarding BALCO Laboratories. BALCO has been working with elite Olympic and professional athletes for over fifteen years. BALCO has provided testing and consultation for over 250 NFL players including the entire 1998 Super Bowl Champion Denver Broncos team and the entire Miami Dolphins team. BALCO works with professional athletes in many sports including teenis (Michael Chang, Jim Courier, etc.), hockey, bodybuilding (10 of the 16 1998 Mr. Olympia contestants), track and field, soccer and basketball (Seattle SuperSonics).
BALCO Laboratories has been testing and monitoring Flex on a routine basis during the last year. We have performed tests including blood chemistry (SMAC), complete blood count (CBC), PSA, anabolic hormone levels, genotyping as well as comprehensive testing for nutritional elements. Flex's test results have been compared to twenty-four other professional bodybuilders and overall he has one of the healthiest profiles. Basically, Flex is in excellent health and has demonstrated the discipline necessary to maintain a peak level of conditioning.
Flex was a participant in a study we recently conducted in collaboration with the Department of Human Genetics at the University of Pittsburgh involving 62 men who made unusually large gains in muscle mass in response to strength training (extreme responders). Flex was one of only nine extreme responders that had the very rare "myostatin mutation." Myostatin is the gene that "limits muscle growth." Specifically, Flex had the rarest form of myostatin mutation at the "exon 2" position on the gene. This simply means Flex has a much larger number of muscle fibers compared to the other subjects or the normal population. We believe that these are the very first myostatin mutation findings in humans and the results of this landmark study have already been submitted for publication. Flex was also found to have a very unusual type of the IGF-1 gene. In fact, Flex was the only participant in the study that did not have a "match." All of the other extreme responders had at least three other subjects with a matching IGF-1 gene. Based upon Flex's very unique genetic profile, we plan to expeditiously publish a scientific paper that reveals his complete genotype in specific detail. The publication of his remarkable genetic data should generate an enormous amount of media exposure.
Hope this information will be helpful and please call if I can be of assistance.
Sincerely,
/s/ Victor Conte
Victor Conte
President
BALCO Laboratories, Inc.
1520 Gilbreth Road • Burlingame, CA 94010 • 1-800-777-7122 • FAX (650) 687-6576
MATERIALS AND METHODS
Sequencing of selected regions of the myostatin gene and genotyping
of common variants were carried out in a comparison sample of
96 randomly selected Caucasian and 96 African American subjects
from the general population. An additional 72 individuals were
screened for a common exon 2 variant. One hundred fifty-three
subjects, including 127 men (32 African American, 91 Caucasian,
and 4 Asian) and 26 women (9 African American, 16 Caucasian, and
1 Asian), were categorized by the magnitude of increases in muscle
mass they experienced from strength training. The subjects consisted
of world-class bodybuilders (ranked in the top 100 worldwide)
(N 5 18; 5 were ranked in the top 10), competitive bodybuilders not
ranked in the top 100 (N 5 25), elite power lifters (N 5 7), university
football players (N 5 9), previously untrained subjects who had their
quadricep muscle volume measured by magnetic resonance imaging
before and after 9 weeks of heavy resistance strength training of the
knee extensors (N 5 33), and nonathletes, who were questioned
about their ability to increase their muscle mass in response to
intense and prolonged strength training (N 5 61). A rating of 5 was
given to those who were world-class bodybuilders and to those who
increased their quadriceps muscle mass by .400 cm3 after only 9
weeks of strength training, whereas a rating of 0 was given to those
who experienced no noticeable increase in muscle mass after vigorous
strength training for at least 6 months. Eighteen subjects received
a rating of 5, and 13 subjects received a rating of 0. The
ratings of the remaining subjects fell somewhere between these two
extremes. Subjects who were rated as either 4 or 5 were classified as
extreme responders (N 5 62) and were compared to those who were
rated as either 0 or 1 and were classified as nonresponders (N 5 48).
Subjects were also grouped and compared by race. Information on
muscle mass changes with strength training from the remaining
subjects was obtained through either estimates of fat-free mass
assessed by dual-energy X-ray absorptiometry or hydrodensitometry
or in the case of competitive bodybuilders, power lifters, football
players, and nonathletes, through questionnaire data on prior success
in bodybuilding competition and/or reported changes in muscle
mass with strength training. Informed consent was obtained from all
subjects under protocols approved by the Institutional Review
Boards of the University of Maryland and the University of Pittsburgh.
Laboratory methods. Genomic DNA was prepared from EDTA
anticoagulated whole blood or from cheek swabs by standard methods
(Miller et al., 1988). DNA amplification primers for each exon and
the 59-flanking region of the human myostatin gene were designed
based on the cDNA sequence of human myostatin (GenBank Accession
No. AF019627) and the genomic organization of the bovine
myostatin gene (Grobet et al., 1997).
it is interesting to note that three of the
African American nonresponders were homozygous for
the less common (Arg) allele at the exon 2 K153R site,
while none of the responders were homozygous for this
allele. Three of the five mutations causing the doublemuscle
phenotype in cattle occur in exon 2 and are
recessive, but two are chain termination mutations
and one is a deletion, expected to produce a nonfunctional
myostatin protein (Grobet et al., 1998). Whether
variation in the myostatin gene influences muscle phenotypes
other than the muscle mass increase in response
to strength training requires further exploration.
1: J Appl Physiol. 2007 Mar 8;
Activin RIIB and Follistatin Haplotype Associations with Muscle Mass and Strength in Humans.
Walsh S, Metter EJ, Ferrucci L, Roth SM.
PURPOSE: Genetic variation in myostatin, a negative regulator of skeletal muscle, in cattle has shown remarkable influence on skeletal muscle resulting in a double-muscled phenotype in certain breeds; however, DNA sequence variation within this gene in humans has not been consistently associated with skeletal muscle mass or strength. Follistatin and Activin RIIB (ACVR2B) are two myostatin-related genes involved in the regulation/signaling of myostatin. We sought to identify associations between genetic variation and haplotype structure in both follistatin and ACVR2B with skeletal muscle related phenotypes. METHODS: Three hundred and fifteen males and 278 females aged 19-90 years from the Baltimore Longitudinal Study of Aging were genotyped to determine respective haplotype groupings based on HapMap data. Whole-body soft tissue composition was measured by dual-energy X-ray absorptiometry. Quadriceps peak torque (strength) was measured using an isokinetic dynamometer. RESULTS: Women carriers of ACVR2B haplotype group 1 exhibited significantly less quadriceps muscle strength (shortening phase) than women homozygous for haplotype group 2 (109.2 +/- 1.9 vs 118.6 +/- 4.1 N.m, 30 degrees /sec, respectively, p = 0.036). No significant association was observed in men. Male carriers of follistatin haplotype group 3 exhibited significantly less total leg FFM than non-carriers (16.6 +/- 0.3 vs 17.5 +/- 0.2 kg, respectively, p = 0.012). No significant associations between these haplotype groups were observed in women. CONCLUSION: These results indicate that haplotype structure at the ACVR2B and follistatin loci may contribute to inter-individual variation in skeletal muscle mass and strength, though these data indicate sex-specific relationships. Key words: genetics, skeletal muscle, myostatin, sex.
PMID: 17347381 [PubMed - as supplied by publisher]
Interview with the doctor from the study
