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Evaluation and control of meat quality in pigs PDF

443 Pages·1987·51.457 MB·English
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3 'mE PHYSIOLOGY AND BIOCHEMISTRY OF mE PORCINE STRESS SYNDJO.1E David Lister Animal and Grassland Research Institute Shinfield, Reading RG2 gAQ, U.K. ABSTRACT Much of the pertinent biochemistry and physiology of the Porcine Stress Syndrome has been defined but a number of key problems have yet to be solved. For example, we do not know why individuals differ in their threshold of sensitivity to stressors, exactly how muscle activ i ty is triggered under these circumstances and why some animals may quickly recover fran such stinruli and others may not. Neither is it completly clear how sensitivity to stressors and body composition are linked. There is, however, good evidence that the syrrpathetic nervous system and the catecholamines of the adrenal R'edulla are essential elements in all of this. P. V. Tarrant et al. (eds.), Evaluation and Control of Meat Quality in Pigs © ECSC, EEC, EAEC, Brussels-Luxembourg 1987 4 INI'RODUCTION The Porcine Stress Syndrome (PSS) has been an important focus in research on pigs and pigmeat for at least 20 years. The research has taken on many guises to include topics as different as genetic polym::>rphisms, animal behaviour, mitochondrial function and the classical approaches of stress physiology. What began as enquiries into the nature of aberrations in meat quality, quickly recognised in the aetiology of the problem the important contribution of genetic type and the ways in which animals were handled, and drew in expertise from animal and meat science. The pig was recognised as a model for certain comparable conditions in man and opened the field for contributions from human medicine. It is fair to say, however, that many of the early prognostications of researchers, especially in regard to associations between the leanness of carcases and the quality of meat, fell on deaf ears and only relatively recently have the pig and meat industries begun to ask whether the search for ever leaner carcases should not be tempered to preserve the vigour of the live animal and the quality of its meat. There have been many reviews of PSS in terms of the associated physiology and biochemistry (Briskey, 1964 ~ Cassens et a1., 1975 ~ Lister et a1., 1981) and little will be served by rehearsing them. Instead I shall attempt to identify the physiological and biochemical issues behind the following questions and raise more questions which require further research. 1. What is PSS? 2. How can PSS be described in objective terms? 3. How is meat quality affected? 4. What makes some pigs stress prone? WHAT IS PSS? All animals (and men) will react characteristically to physical, mental and environmental stressors and, if those stressors are particularly severe, individuals may die. Within species, stress prone lines have been identified and perpetuated by breeding. It may be considered that PSS represents the perpetuation of such proneness ruoongst pigs which have been selected and bred primarily for, for example, rapidity and efficiency of growth, or body composition 5 and conformation, but which also contain undesirable characteristics which may be called 'stress proneness'. Typically Pietrain, Poland China and strains of Landrace pigs have been noted for their dramatic and often fatal reactions to such stimuli as transportation, raised environmental temperature and physical exercise, restraint or general handling (Topel et al., 1968). This porcine stress syndrome is characterised by muscle treroc>r, an increased respiratory rate, a systemic acidosis and a rise in body temperature. After the animal dies, or if it is slaughtered in the reacting state, rigor roc>rtis develops alroc>st immediately to give rise to the characteristic pale, soft and exudative (PSE) condition of the meat. Fatal responses to environmental stress are to be found aIrongst several species of animals. Capture myopathy is a condition which develops in wild animals such as antelopes and buffaloes being pursued and captured for whatever reason and many will die (Harthoom et al., 1974). Clinical symptoms and post roc>rtem findings are similar to those of PSS. Malignant Hyperthermia (MH) which develops in certain pigs (and people) when they are exposed especially to the halogenated gaseous anaesthetics, but also spontaneously during stressful encounters, is another reaction which has been incorporated into the general condition referred to as PSS (Nelson et al., 1974; Lucke et al., 1979). MH has been particularly important in defining the physiological and biochemical events in PSS for it is possible to precipitate MH under laboratory conditions and thereby allow detailed roc>nitoring of blood and tissues throughout the reaction. HOW CAN PSS BE DESCRIBED IN OBJECTIVE TERMS? The first steps towards characterising PSS were made in the late 1960s when attempts were made to identify the metabolic events in muscle or roc>re generally associated with the exposure of animals to various and extreme environmental conditions (Kastenschmidt et al., 1965; Forrest et al., 1968; Kallweit, 1969). In some studies (Judge 1969) a period of exercise was included in addition to thermal stress. Results from these experiments paved the way for the roc>re sophisticated approaches of later studies which for the roc>st part only confirmed the earlier findings. Temperature stress, it seems, is likely to lead to respiratory alkalosis which becomes a metabolic acidosis if exercise is included as a treatment. 6 The extent of the reaction to these stressors, and particularly the ability of animals to maintain or recover homeostasis, was used to identify so-called stress-susceptibility or -resistance anongst the experiroontal pigs. This terminology has become comm::mplace in the literature but generally refers to breeds e.g. Poland China, stress susceptiblej Chester White, stress-resistant. In recent tiroos this nomenclature has been refined with the introduction of the terms Halothane-positive or -negative which may be used to describe animals within as well as between breeds. It is generally accepted that the pattern of metabolic, physiological and biochemical developments in MH is very similar to, if not the same as, that which occurs as a response to environmental stress. The MH reaction has been extensively characterised in the literature (Berman et al.,1970j Hall et al.,1980j Gronert,1980) and only a short description is necessary here. Essentially, the characteristic signs of MH (and stressor induced reactions generally) are increased oxygen consumption and carbon dioxide production. The developing respiratory and metabolic acidoses are associated with high plasma lactate levels and falling pH. Glucose and fat mobilisation (as identified by plasma glycerol concentration) occur, though plasma free fatty acids may fall. There are substantial electrolyte changes and some haemoconcentration. Contrary to the early views, rruscle stirrulation which is the primary source of heat production in MH (Hall et al., 1976) is fuelled almost if not wholly via aerobic metabolism and it is only in the later stages that this contribution declines to less than 50 per cent. Another early view was that cardio Il¥opathy contributed to the demise of stress-prone pigs. There is, however, no functional evidence for this for the hearts of pigs suffering MH appear to respond adequately to metabolic demand even when there is substantial acidosis and hyperkalaemia. Only in the later stages does cardio vascular function become limiting. At this tiroo cyanosis of the skin, resulting fram peripheral vasoconstriction, is associated with reduced heat loss, reduction in substrate provision and lactate clearance from tissues and as the biochemical changes reach extreme values, blood pressure falls and cardiac arrest occurs. All these changes are familiar findings in the terminal stages of the Porcine Stress Syndrome. 7 HCM IS MEAT QUALITY AFFECTED? The consequences of PSS post oortem can be either the accelerat ion of the nomal biochemical changes which occur during the rigor process or their curtailment, leading in the first instance to pale, soft and exudative (PSE) meat and, in the second, to dark, firm and dry (DFD) meat. In the living animal, metabolism is sustained through adenosine triphosphate (ATP) production, predominantly via aerobic means, using glucose and fatty acids as substrates. At times, demand is such that aerobiosis is insufficient to meet metabolic needs for ATP. This occurs in the classical fight/flight reactions when anaerobic glycolysis provides for an increasing proportion of energy needs. Though this process is only approximately 5% as efficient in the production of ATP as aerobic processes, it is nevertheless an important source of energy for emergency needs and the sole I I mechanism employed in the transition of living IlD.lscle to dead meat. The two systems in muscle cells which control these changes are the glycolytic system which converts glycogen to lactate and those processes which lead to the dephosphorylation of ATP. Acidification occurs as a consequence of glycolysis: rigor, as a result of the loss of ATP. The series of reactions which regulate all this is described by Bendall (1973). It is important to recognise this interdependence of glycolysis and the production of lactate and the enzymic processes in living muscle whose function is to synthesis ATP from adenosine diphosphate (ADP) and inorganic phosphate in anaerobic conditions. In fast I I muscles, the production of sufficient pyruvate for mitochondrial oxidation requires only a small fraction of the glycolytic enzymes present; the large excess of these enzymes exists for anaerobic circumstances. The freely reacting adenine oononucleotides exist alm::>st entirely as ATP and glycolysis can occur only as long as ADP is being produced by an ATPase system. Ultimately, therefore, the rate of glycolysis is determined by ATPase activity and not directly by the activities or amounts of glycolytic enzymes or hormones. In the ini tial stages of a surge in demand for ATP or in the post mortem period, phosphocreatine, which is present at high levels initially, provides for the re-conversion of ADP (produced by ATPase activity) to ATP. Glycolytic phosphorylation of ADP becomes increas- 8 ingly ~rtant as the concentration of phosphocreatine falls. The first reactions of glycolysis produce enough substrate to remove ADP at the rate it is formed but there is no suggestion that the concentration of ADP is rate limiting. Control is achieved via feed back on both phosphorylase and phosphofructokinase activity by the adenosine monophosphate (AMP) level which in turn is regulated by AMP deaminase. This enzyme is also primarily responsible for the simultaneous accumulation of inosine monophosphate (IMP) and depletion of AMP especially at pH<6.5. The action of myokinase restores the lost AMP via ADP which in turn is restored by ATPases and a consequent reduction in ATP concentration. Glycolysis stops and the ultimate pH is reached when there is no freely reacting adenine mononucleotide in the muscle. Glycolysis will also stop at an abnormally high pH (DFD meat) when all glycogen has been depleted from muscle. This implies inadequate stores of glycogen at death for normal rigor will continue to the usual ultimate pH (N5.5 at which there may be 'residual' glycogen in muscle. In this case the exact determinant of ultimate pH Le. the point at which glycolysis stops is not clear. It seems likely however that AMP deaminase is primarily responsible since it represents the sole cause of loss of adenine nucleotides. From this it can be concluded that variations in the rate and extent of pH fall are attributable to the controls exercised before and after death by ATPases and AMP deaminase. The problems arise in identifying the physiological basis for these activities. The practical consequences of these biochemical changes are the PSE and DFD conditions of pigmeat. Rigor mortis takes place in pig muscle over a period of about 10 hours during which the pH has fallen fran about 7.3 to 5.5. On occasion this change may occur wi thin a few minutes of death and the meat develops the pale, soft and exudative characteristics. The classical explanation for this has been • thenroprotonic stress (Scopes, 1964) which occurs when the pH of I muscle falls below 6.0 and its temperature is >300C. Under these conditions extensive denaturation of the soluble and structural proteins occurs which leads to a loss of their water binding abilities and the precipitated prot~ins interfere with the optical properties of the muscle to cause more incident light to be reflected and a paler appearance. Penny (1975) suggested that during normal rigor, drip came from the extracellular water compartment which became enlarged as the 9 et al.'s (1984) finding that rabbit l.dorsi fibres swelled to two to three times their usual diameter when inroorsed in hypertonic salt solutions and, like Offer & Trinick's (1983) observations, was explained by myofibrillar swelling. Wilding et ale (1984) also concluded that myofibrillar swelling was constrained by the endomysial sheaths around fibres. It is now proposed (see Offer, 1984) that drip formation during rigor mortis represents the redistribution of extra and intra cellular water and the expulsion of part of the extracellular component out of the cut ends of meat close to the perimysium, probably as a result of internal pressure exerted by the connective tissue network and disruption of cell membranes (Currie & w)lfe, 1983) • This explanation does not require there to be a change in the total water content of muscle prior to an animal's death. It is, however, quite possible, indeed likely, that quite sizeable changes occur in the fluid compartments in the body prior to death, especially if there are profound metabolic and physiological disturbances happening simultaneously (Guyton et al., 1975). Lister et ale (1985 - in preparation) recently examined this proposition in halothane sensitive pigs of the Lacombe breed. During MH reactions precipitated by halothane and suxamethonium administration, the typical changes in muscle and rectal temperature occurred, the haematocrit rose and plasma volume fell. The pH of biopsy samples of muscle fell and amounts of expressible juice and the turbidity of extracts of muscle increased. Moreover, the water content of the muscle samples at death was higher in reacting pigs than in non-reacting control animals. Thus at least a proportion of the drip released by PSE muscle may well be attributable to the increase in intracellular fluid volume which accompanies the development of MH and, probably, PSS. DFD meat is the condition which affects meat which remains at pH>6.0 - 6.3 when there is insufficient glycogen available in muscle at death to allow the full development of acidification to occur. The premature depletion of muscle glycogen in stressed animals is not easily explained. It is not induced simply by fasting, exercise or a combination of the two; mixing groups of animals even for a short period may, however, bring it about. Tentative explanations may be found by examining the mechanisms which allow muscle LO function under a variety of phvsioloqical states. 10 The concentration of glucose in the blood of animals is maintained within fairly constant limits even though there might be fluctuations in the storage and nobilisation of nutrients which are associated with feeding and activity. Even under resting conditions, however, activity can only be maintained for relatively short periods if carbohydrates (derived from liver glycogen in the main) are the sole source of energy. For longer periods of activ i ty, the long chain free fatty acids (FFA) nobilised fran adipose tissue are employed (Newsholme, 1980) which progressively, as activity intensifies, cause a reduction in glucose utilisation by muscle. The control over this balance is thought to be exercised by fatty acid oxidation and due in part to the inhibitory effect of citrate on the enzyme phosphofructokinase. A further increase in the workload will reduce the concentration ratio ATP/ADP and glycolysis is stimulated at the expense of stores of muscle glycogen. A continuing ability to mobilise fatty acids and the maintenance of aerobiosis is thus of the utmost importance for sustained activity. Hall et ale (1980) showed that in MH reactions, the continued use of free fatty acids for energy purposes can be prejudiced. Lipolysis is stimulated during MH under the influence of catecholamines, but plasma FFA concentrations may fall as a consequence of their re esterification during the developing acidosis. Because the utilis ation of FFA is determined by their concentration in plasma, the continued energy demand of the reaction must be met ultimately by muscle glycogen. Thus one might conclude that the loss of muscle glycogen and predisposi tion to Dm by stressed animals is a natural consequence of continued muscular stimulation when the supply of other energy substrates, notably FFA, is reduced. WHAT MAKES PIGS STRESS PRONE? It can be concluded from much of the above that many of the symptoms of PSS are the consequences of profound muscular stimulation. It may well be also that such stimulation not only provides the symptoms of PSS but also the ease with which this occurs, conditions whether pigs become stress susceptible or resistant. The rate of glycolysis in muscle, occurring either before death or during rigor nortis, is determined by ATPase dctivity and not 11 directly by the activities or amounts of glycolytic enzymes or hormones. Stress proneness, therefore, amounts to the ease with which IIllsc1e is stiIru1ated and how readily recovery can be established. There seems to be general agreement, though a dearth of evidence, that the ultimate triggering mechanism resides in nusc1e itself. However, no major rrorpho1ogica1 differences have been identified in muscle except evidence of myofibri11ar damage and regeneration (Muir, 1970; Venable, 1973). Swat1and and Cassens (1972) described various abnormalities in the peripheral innervation of striated nusc1e though no functional abnormalities have been recognised. Defects in the ability of nusc1e components to handle ea++ have ++ long been suspected but rarely demonstrated, though the role of ea in the stinu1ation of myofibrillar ATPases and phosphorylase kinase nust be of potential importance. The sarcoplasmic reticulum was thought to have impaired function though it is likely that this could be explained by experimental artefact (Greaser et a1., 1969) (though see Heffron - this volume). Halothane sensitive pigs appear to have higher sarcoplasmic ea++ levels than normal (Cheah & Cheah, 1984) and this has been linked with significantly higher activity of Ca ++ activated phospholipase ~(EC 3.1.1.4) (Cheah & Cheah, 1981). This in turn leads to the enhanced release of mitochondrial Ca++. More recently Cheah & Cheah (1984) suggested that the enhanced phospholipase ~ activity was due to the higher concentrations of endogenous calrrodu1in in sensitive pigs. Even via these postulated mechanisms, a means has yet to be identified of switching on the aberrant behaviour of IIllsc1e in MH or PSS. Monnede and Lentzer (this volume) propose that behavioural responses to stressful environmental factors in intensive pig husbandry are prime factors in the aetiology of PSS. It is certainly true that environmental stressors affect the incidence of PSS and PSE meat but anaesthesia or tranquillisation substantially rrodifies the incidence of PSE only arrongst those animals which are not genetically prone to the PSS condition (Briskey & Lister, 1969). \'hat matters then, is the inherent mechanism which sets the threshold of sensitivity in pigs to make them more or less liable to develop PSS. The role which the sympathetic nervous system and the adrenal gland play in stress responses generally (see Usdin, Kvetnansky and Kopin, 1976) and MH in particular (Hall, 1976) has been very well 12 documented • In MH, catecholarnines appear primarily to prarote the developing reaction via ct + 8 adrenergic responses, but pre-treatrrent with ~ adrenergic blockers or agonists can prevent or initiate a fatal MH response (Lister et al., 1976: Hall et al., 1977). The combination of effects Irediated by the main adrenoreceptors can account for the majority of the metabolic events seen in MH and PSS. 8 receptors, for example, are associated, inter alia, with increased liver glycogen olysis and vasoconstriction, 8 receptors with heart rate and fat 1 mobilisation, and 82 receptors with muscle glycogenolysis and vaso dilation. The use of receptor specific drugs has allowed us to clarify the particular mechanisms of relevance within PSS and MH. ct blockade clearly prevents the development of MH in sensitive pigs whereas 8 blockade with propranolol (Lister et al., 1976) or carazolol (S.Lens - personal comnnmication) does not. The development of PSE meat can be impeded by ct blockade, though not substantially, and treatrrent with propranolol may also have a slight beneficial effect (Lister, 1974). Warriss & Lister (1982) have provided clear evidence, however, of the effectiveness of carazolol in reducing the incidence of PSE in stress susceptible Pietrains. Carazolol, like propranolol, is described as a non-specific 8 blocker but Warriss & Lister's findings allow a clear distinction to be drawn between MH and aspects of PSS such as PSE meat. rhatever the specific mechanism is which triggers MH in the living pig,it is not the same as the trigger for the production of PSE meat' although that might represent a further part of the continuum of adrenergic reactions which constitute PSS. The contribution identified for the sympathetic nervous system in MH and PSS suggests mechanisms which link up with the other notable feature of the syndromes i.e. the leanness of susceptible individuals. Pietrain pigs are thought to develop their leanness through enhanced responsiveness to the fat mobilising effect of noradrenaline (Wbod et al., 1977). For such a mechanism to contribute to leanness in the growing animal, the adipose tissue of lean pigs would have to be exposed to levels of noradrenaline which were higher than those found in fatter types, or the appropriate adrenergic receptors present in greater concentrations. Gregory & Lister (1981), using a Valsalva-

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