The effect of the dietary status of vitamin A on carbohydrate metabolism, postmortem isometric tension development, and shear resistance of Pectoralis major muscle was studied. Depletion studies conducted over a 5-week period indicated a definite influence of vitamin A deficiency on muscle carbohydrate metabolism. Mild hypovitaminosis A induced an increase in glycogen deposition, whereas severe deficiency led to a reduction of these elevated stores. Vitamin A deficiency did not affect the ability of P. major strips to develop isometric tension postmortem. The P. major strips sampled from deficient cockerels generally required longer to reach maximum tension than those of controls. The extended times to maximum tension reflected an increased muscle glycogen content. A significant increase in shear value similarly corresponded to the increased myofibrillar contraction noted in the later deficiency stages. Cockerels which had previously received for five weeks a ration completely deficient in vitamin A were utilized for a two-week repletion study. Although there was a distinct delay in response to the feeding of a vitamin A adequate ration, the muscle glycogen content, isometric tension parameters, and shear values of repleted birds were similar to those of controls within the two-week period.
Commercial chicken broilers were fed a semipurified diet deficient in vitamin E and selenium from day 1 to day 13 ex ova and subsequently fed varying levels of dietary selenium and vitamin E. All birds were sacrificed on the 28th day, stored for 36 hr at 2 C to allow the onset and resolution of rigor, and frozen at -32 C until needed. Total cathepsin content of the Pectoralis major depended upon dietary vitamin E for birds receiving 0 to 12 IU/kg, whereas selenium administered at .05 to .16 ppm in the diet showed no statistically significant effect. Similarly, total protein content of P. major increased with increasing level of dietary vitamin E, but the level of dietary selenium had no effect. Muscle break strength was significantly affected by dietary selenium and vitamin E (P = .0092) interacting together. Catheptic activity and muscle protein explained 6.36% and 3.58% of the viriability in muscle break strength. Birds with more advanced avian white muscle disease showed higher break strength values. Ultrastructural deterioration of the myipathic muscle included disintegration of blood vessel walls, transverse tubules, and mitochondrial membranes as well as the obvious disruption of the myofibrillar components. Myelin figures were present in diseased, but not in normal, muscle. Accumulation of adipocytes both extracellularly and intracellularly occurred in selenium and vitamin E-deficient birds.
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