Double Muscling in Cattle: Genes, Husbandry, Carcasses and Meat.

Molecular biology has enabled the identification of the mechanisms whereby inactive myostatin increases skeletal muscle growth in double-muscled (DM) animals. Myostatin is a secreted growth differentiation factor belonging to the transforming growth factor-β superfamily. Mutations make the myostatin gene inactive, resulting in muscle hypertrophy. The relationship between the different characteristics of DM cattle are defined with possible consequences for livestock husbandry. The extremely high carcass yield of DM animals coincides with a reduction in the size of most vital organs. As a consequence, DM animals may be more susceptible to respiratory disease, urolithiasis, lameness, nutritional stress, heat stress and dystocia, resulting in a lower robustness. Their feed intake capacity is reduced, necessitating a diet with a greater nutrient density. The modified myofiber type is responsible for a lower capillary density, and it induces a more glycolytic metabolism. There are associated changes for the living animal and post-mortem metabolism alterations, requiring appropriate slaughter conditions to maintain a high meat quality. Intramuscular fat content is low, and it is characterized by more unsaturated fatty acids, providing healthier meat for the consumer. It may not always be easy to find a balance between the different disciplines underlying the livestock husbandry of DM animals to realize a good performance and health and meat quality.