October 27, 2011
CLAY CENTER, Nebraska: The secrets of how to produce a guaranteed tender steak every time continue to be elusive.
Research at the ARS Roman L. Hruska Meat Research Center (MARC) has found that meat tenderness is only 50% due to the genetics of the animal. The rest is the result of non-genetic factors such as stress and diet.
Research by Mohammad Koohmaraie and feed technologist Tommy L. Wheeler in the 1980s found that the tenderness of meat changes during the port mortem aging - first going through a toughening phase before the tenderization phase begins.
Right after slaughter, meat is tender. But for the next 12 hours or so, rigor mortis takes place, stiffening the muscles and making the meat tough.
Toward the end of the toughening phase, while the carcass is hanging in the cooler, the tenderization phase begins, which makes most meat - but unfortunately not all - suitably tender.
The researchers found that steaks sold before 14 days of aging are more likely to be tough. Such long aging is very costly due to the large amount of cooler space this requires and has been resisted by the commodity beef processors.
Even worse, the 14 day aging still does not “guarantee” a tender steak and some will still be unacceptably tough.
It was hoped that a genetic “magic bullet” could be found that eliminate the need for aging.
It was discovered at MARC that tenderization was caused by the enzyme u-calpain which degrades some muscle proteins. However, u-calpain requires calcium to be present to do this.
Koohmarie and Wheeler have developed a process of calcium marination that has both improved meat tenderness and juiciness. Again, this has also been resisted by the beef processors as it slows down their inventory turnover.
Subsequent research discovered that while u-calpain causes the protein degradation that improves meat tenderness, its actually the activity of a protein called calpastatin that determines how much calpain is active - and thus how tender the steak will be.
However, attempts to develop a tenderness classification system based upon calpastatin activity have not been successful. This is because calpastatin explains only 45% of the variation in tenderness, which is not high enough for accurate classification.
A complimentary genetic program have tried to identify gene markers for u-calpain.
These have been thwarted by the heavy use of crossbred beef animals in the USA but u-calpain gene markers have been developed for the most popular purebred beef breeds.
However, research indicates that there may be many genes other than u-calpain and calpastatin that influence tenderness - albeit at lesser effect. As a result many more genetic markers will be required to explain enough of the variation to accurately guide breeding choices.
“There is only so much we can do with genetics, “ chemist Timothy Smith of MARC said.
“The rest is determined by how the animal and the meat are handled throughout the various steps of beef production.”
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