Graham Gardner

Genetic selection for lower fatness is commonly practiced in sheep breeding programs to improve consumer appeal for sheep meal products. This selection strategy may result in changes to glucose production. In particular liver glucose output, which is of particular importance for breeding Merino ewes since then ability to build energy stores in nutritionally marginal environments is paramount for reproductive success. Hepatic glucose output can be measured by administering controlled doses of adrenaline which is a strongly catabolic hormone that among other things stimulates the liver to rapidly increase the output at glucose. This release of glucose is the net result of adrenaline-stimulated mobilisation of stored glycogen combined with glucose synthesis from gluconeogenic precursors. The rate of gluconeogenesis in response to adrenaline may he higher in genetically fat sheep as both the basal and adrenaline-stimulated rates of glucose synthesis are higher in genetically fat rats (Rohner—Jeanrenaud et al., 1986. Sanchez-Gutierrez et al., 2000) Furthermore, obese humans have higher rates of gluconeogenesis and higher concentrations of hepatic glycogen than their lean counterparts, both of which would favour greater glucose release in response to adrenaline (Muller et al., 1997). Thus we hypothesise that glucose output following an adrenaline challenge will be lower in ewes that are genetically leaner.

The quantity of glycogen stored in muscle at slaughter is a major determinant of meat quality and profitability. Muscle glycogen levels below ~0.6% can result in high ultimate pH (>5.7) of beef (Ferguson el al. 2001) leading to dark cutting or dark firm dry (DFD) meat. Meat which is DFD has a darker colour, reduced shelf life, bland flavour and variable tenderness (Ferguson el al. 2001). This condition significantly reduces the value of a carcase since an elevated ultimate pH (>5.7) makes it ineligible for grading by Meat Standards Australia and premiums will not be rewarded. Low muscle glycogen pre-slaughter is caused by low glycogen storage as a result of low metabotisable energy intake Knee el al, 2004) and/or stress between mustering and slaughter. Stress stimulates the release of endogenous adrenaline, causing the mobilisation and depletion of muscle glycogen stores. When glycogen stores are low, stressors have the greatest influence on the incidence of DFD meat.

The demand for more profitable, high yielding carcasses by the beef industry has increased selection for animals with more muscle and less fat. Animals that have increased muscle hypertrophy generally have more fast-glycolytic type IIX myofibres (Wegner et al., 2000). The adrenaline responsiveness of muscle with more fast- glycolytic fibres is likely to be greater due to their increased glycolytic and glycogenolytic capacity (Wegner et at. 2000), possibly extenuating the problem of DFD meat in high muscling selection line cattle. Therefore, we hypothesise that selection for muscling will decrease muscle glycogen storage and increase the response of muscle to adrenaline.

Australia produces beef cattle for export markets which require meat to have high marbling and intramuscular fat contents. In order to produce such meat qualities cattle are fed high energy grain based diets for extended periods of time. Compared to cattle on pasture based roughage diets, cattle on high concentrate rations may be exposed to increased heat loads due to increased heat production from digestion and metabolism of the high energy diet.

This paper discusses the management of consumer defined beef palatability using a carcass grading scheme which utilizes the concept of total quality management. The scheme called Meat Standards Australia (MSA) has identified the Critical Control Points (CCPs) from the production, pre-slaughter, processing and value adding sectors of the beef supply chain and quantified their relative importance using large-scale consumer testing. These CCPs have been used to manage beef palatability in two ways. Firstly, CCPs from the pie-slaughter and processing sectors have been used as mandatory criteria for carcasses to be graded. Secondly, other CCPs from the production and processing sectors have been incorporated into a model to predict palatability for individual muscles. The CCPs from the production (breed, ossification and implants of hormonal growth promotants), pre-slaughter and processing (pH/temperature window, alterative carcass suspension, marbling and ageing) sectors are reviewed. The paper then discusses the interacting roles of nutrition and genotype as determinants of muscle energy pattern with respect to glycogen and fat metabolism. In particular the roles of fibre type and/or pattern of muscle energy metabolism is discussed in relation to the high ultimate p11 syndrome (dark cutting beef), the rate of post mortem glycolysis and the response to electrical stimulation. Finally the development of intramuscular fat is discussed in terms of growth and development, biochemical regulation and nutritional modification.