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.