In regard to double muscling, I checked out a research paper entitled Double Muscling and Myostatin. Again, since I know little if anything about it and nobody has really answered my questions, I looked them up for myself.
According to the research cited, double muscled cattle have 10% less bone, are higher in polyunsaturated fats, 11% to 5%, have significant carcass advantages compared to non double muscled cattle. There are associated reproduction, growth, and fatigue issues, though.
Angus sired cattle with one copy of the myostatic gene had significantly increased carcass weight, muscle conformation score, and rib eye area, but it had no effect on fat traits. Another study based on Angus sired cattle with only one copy of the gene showed greater yield, 67% to 63%, less fat trim, 15% to 18%, larger rib eye area, 85 cm2 to 73 cm2, with no difference in P8 and rib fat depths or in marbling scores. The conclusion was that breeding programs that utilize 1 heterozygous parent can increase beef yield by 3.5% with no significant adverse effects. Opponents argue improved carcass quality improvement (resulting from 1 copy of the myostat gene) comes at the expense of reproduction. Research proves this false. There are significant advantages to be gained from breeding heterozygous animals due to their increased beef yield and meat quality.
The research says that the myostatin gene is not the only gene involved in double muscling syndrome. Although the myostatin gene has a considerable effect, other more subtle effects are involved in the expression of the phenotype. The same myostatin is found in Belgian Blue, Piedmoteise, and South Devon. However, South Devon do not exhibit the physical characteristics as often or to the extent. The reason for the variability in phenotypic expression lies in the fact that the effects of the myostatin gene appear to be influenced to a greater or lesser extent by a number of other, as yet unidentified genes. While the defective myostatin gene has been found in a number of European beef breeds, the only British beef breed in which it occurs in any frequency is the South Devon. This is because breeders have been selecting for additional muscling, but avoiding the extreme double-muscled phenotype. Thus, almost by coincidence, they have selected not only for the defective myostatin gene, but also for those other modifying genes with the result that significant numbers of the breed (2/3) now carry the defective myostatin gene (with its associated advantages) but do not present the problems posed by those breeds with more extreme double muscling.
From this research, one could conclude that one copy of the myostatin gene has several advantages. The myostatin gene alone is not responsible for the double muscling phenotype, there are other as yet unidentified genes. Maybe if we have suspected carriers of the myostatin gene, we should wait for more information before we kill or discard them. If they have everything else we want, with a little extra muscling and the other positive attributes riding along with 1 myostatin gene, why throw the baby out with the bath?
Another source said the University of Alberta had double muscled Angus in the 60's. The likely source, according to the article, was the Fresian (Holstein). Their language, not mine.
