R. I. Richardson

Bio: R. I. Richardson is an academic researcher from University of Bristol. The author has contributed to research in topics: Polyunsaturated fatty acid & Intramuscular fat. The author has an hindex of 28, co-authored 69 publications receiving 8095 citations.

Manipulating meat quality and composition.

Abstract: Meat quality describes the attractiveness of meat to consumers. The present paper focuses on two major aspects of meat quality, tenderness and flavour. Both aspects of quality can be influenced by nutrition, principally through its effects on the amount and type of fat in meat. In several countries, high levels of intramuscular fat (marbling fat), i.e. above 30 g/kg muscle weight in longissimus, are deemed necessary for optimum tenderness, although poor relationships between fat content and tenderness have generally been found in European studies, where fat levels are often very low, e.g. below 10 g/kg in UK pigs. Muscle lipid may be a marker for red oxidative (type 1) muscle fibres which are found at higher concentrations in tender muscles and carcasses. Nutritional treatment can be used to manipulate the fatty acid content of muscle to improve nutritional balance, i.e. increase the polyunsaturated (PUFA): saturated fatty acid value and reduce the n-6:n-3 PUFA value. Increasing PUFA levels may also change flavour because of their greater susceptibility to oxidative breakdown and the generation of abnormal volatile compounds during cooking. This situation particularly applies to the n-3 PUFA which are the most unsaturated meat lipids. In pigs, a concentration of 3 mg alpha-linolenic acid (18:3)/100 mg in muscle and fat tissue fatty acids can easily be achieved by including whole linseed in the diet. This level has led to abnormal odours and flavours in some studies, but not in others. In cattle and sheep, feeding whole linseed raised 18:3 concentrations in muscle fatty acids from about 0.7 mg/100 mg to > 1 mg/100 mg. As with pigs, this diet also increased levels of long-chain n-3 PUFA formed from 18:3, including eicosapentaenoic acid (20:5). Although this increase led to greater oxidative breakdown of lipids during storage and the generation of large quantities of lipid-derived volatile compounds during cooking, there were no deleterious effects on odour or flavour. When 18:3 levels are raised in lamb and beef because of grass feeding, the intensity of the flavours increases in comparison with grain-fed animals which consume and deposit relatively more linoleic acid (18:2). In ruminants, very high levels of 18:2 produced by feeding protected oil supplements cause the cooked beef to be described as oily, bland or pork-like.

Myostatin, a negative regulator of muscle growth, functions by inhibiting myoblast proliferation.

Abstract: Myostatin, a member of the transforming growth factor-β (TGF-β) superfamily, has been shown to be a negative regulator of myogenesis. Here we show that myostatin functions by controlling the proliferation of muscle precursor cells. When C2C12 myoblasts were incubated with myostatin, proliferation of myoblasts decreased with increasing levels of myostatin. Fluorescence-activated cell sorting analysis revealed that myostatin prevented the progression of myoblasts from the G1- to S-phase of the cell cycle. Western analysis indicated that myostatin specifically up-regulated p21Waf1, Cip1, a cyclin-dependent kinase inhibitor, and decreased the levels and activity of Cdk2 protein in myoblasts. Furthermore, we also observed that in myoblasts treated with myostatin protein, Rb was predominately present in the hypophosphorylated form. These results suggests that, in response to myostatin signaling, there is an increase in p21 expression and a decrease in Cdk2 protein and activity thus resulting in an accumulation of hypophosphorylated Rb protein. This, in turn, leads to the arrest of myoblasts in G1-phase of cell cycle. Thus, we propose that the generalized muscular hyperplasia phenotype observed in animals that lack functional myostatin could be as a result of deregulated myoblast proliferation.