Limousin myostatin F94L variant affects semitendinosus tenderness.

Texture parameters (peak force and compression), muscle myofibre diameter, and hydroxyproline were measured in semitendinosus samples from a cattle gene-mapping herd. The data were analysed to determine the relationships between these traits. The traits were also mapped by genetic linkage analysis to identify quantitative trait loci, and hence, candidate genes for these traits. Neither texture parameters were affected by the muscle structural traits of myofibre diameter or collagen content (as measured by hydroxyproline), despite significant variation in these traits between animals. QTL for the texture parameters of peak force and compression, as well as collagen content, were found on cattle chromosome 2 (BTA2) and attributed to the myostatin gene. Within the cattle population used for the QTL mapping, a gene variant of myostatin, F94L, has been previously shown to increase muscle mass, predominantly in the semitendinosus. It was determined herein that the F94L myostatin homozygous animals had more tender meat as measured by both peak force and compression. The variant was also responsible for a reduction in the collagen/elastin content of muscle. The myostatin F94L variant had no effect on muscle myofibre diameter of the semitendinosus, even though the variant causes substantial increases in muscle mass. Consequently, the increase in muscle mass of the variant must be due to myofibre hyperplasia and not hypertrophy. In addition, myostatin effects on tenderness are caused by changes in the extracellular matrix rather than muscle myofibre diameter.