Supplementary alpha-tocopheryl acetate (vitamin E) was fed to provide none (E0), 2,000 IU/d (E2000), 5.8 IU/kg live weight (E5.8), or 8.6 IU/kg live weight (E8.6) to steers that were individually fed mainly a corn diet. Three steers were placed on each of 10 treatments: E0, E2000, E5.8, E5.8 to d 126 then E0 to d 266, E0 to d 126 then E5.8 to d 266, E8.6, grazing followed by either E0 or E8.6 all with Holstein steers; and E0 and E2000 with crossbred beef steers. During the last 100 d, vitamin E consumption (International Units/day) averaged 96 for E0, 1,840 for E2000, 2,520 for E5.8, and 3,610 for E8.6. Concentrations of alpha-tocopherol in plasma and in liver and longissimus lumborum biopsy samples obtained every 42 d were elevated (P < .01) by vitamin E supplementation. Tissue saturation was approached at these vitamin E intakes causing similar incorporation of alpha-tocopherol with both per day and per BW supplementation strategies. Maximum accretion or depletion of alpha-tocopherol in plasma and liver occurred before 42 d, but accretion required 120 d and depletion required 180 d in longissimus lumborum. Vitamin E supplementation elevated (P < .01) concentrations of alpha-tocopherol in liver, lung, subcutaneous fat, omental fat, perirenal fat, kidney, diaphragm, spinal cord, longissimus lumborum, and plasma at slaughter with maximum accretion achieved (P < .01) in lung, subcutaneous fat, kidney, diaphragm, and spinal cord. Depletion was not achieved in longissimus lumborum and spinal cord (P < .01), subcutaneous fat (P < .06), and perirenal fat (P < .08) within 140 d. Vitamin E inhibited (P < .01) oxidation at the surface and center of longissimus lumborum steaks displayed for 19 d. Lipid oxidation occurred throughout E0 steaks, but metmyoglobin accumulation occurred more rapidly (P < .01) on the surface than in the center. Myoglobin and lipid oxidation were not concurrent events. Supplementation with vitamin E increased (P < .01) alpha-tocopherol concentrations in longissimus lumborum fractions (mitochondria, microsome, cytoplasm, connective, and remainder) but, except for connective tissue, the proportional distribution of total longissimus lumborum alpha-tocopherol was not affected (P > .1) by vitamin E supplementation. Vitamin E supplementation for at least 44 d at 1,300 IU/d is expected to incorporate adequate amounts of alpha-tocopherol into muscle (3.3 micrograms/g for longissimus lumborum) to produce beef with extended color and lipid stability.

The occurrence of respiratory alkalosis and potential benefit derived from treatment were examined in thermostressed 4-week-old broiler chicks. Blood pH was greater (P less than .05) in heat-stressed (32 C) panting birds (7.395) than either nonpanting (7.28) or birds raised at 24 C (7.28). Acute thermostress, obtained by elevating ambient temperature from 32 to 41 C over a 20-min period further elevated (P less than .05) blood pH to 7.521. Chronic heat-stressed broiler chicks suffer from intermittent respiratory alkalosis during panting; with acute heat stress, chicks pant continuously and suffer from alkalosis. Including .5% sodium bicarbonate (NaHCO3) in the diet of birds subjected to chronic heat stress enhanced body weight gain by 9% even though it tended (P less than .10) to increase blood pH in nonpanting birds. Adding .3 or 1% ammonium chloride (NH4Cl) to diets decreased blood pH (P less than .01) to 7.194 and increased (P less than .05) body weight gains by 9.5 and 25%, respectively. Effects appeared linear with NH4Cl dose to 1% NH4Cl, but 3% NH4Cl elevated weight gains by only 8% and precipitated blood acidosis (pH 7.09) in nonpanting birds. Supplementing the 1% NH4Cl diet with .5% NaHCO3 increased weight gains an additional 9%. Manipulating sodium: chloride ratios by addition of calcium chloride increased body weight gain 8% and slightly reduced severity of alkalosis. Data indicate that blood alkalosis limits growth rate of broiler chicks reared under chronic thermostress and that the respiratory alkalosis and weight gain depressions attributed to thermostress can be partially alleviated dietarily.

Three experiments were conducted to examine the effects of vitamin E supplementation on feedlot cattle. Vitamin E supplementation did not affect feedlot performance or carcass characteristics of cattle fed a high-concentrate diet (P greater than .1). The major finding was the effectiveness of vitamin E in extending the color stability of displayed beef (P less than .01). Color stability during display of longissimus lumborum steaks from cattle supplemented with 300 IU/d for 266 d, 1,140 IU/d for 67 d, or 1,200 IU/d for 38 d was extended by 2.5 to 4.8 d. Gluteus medius steaks had an extended color display life of 1.6 to 3.8 d. The accumulation of lipid oxidation products, but not aerobic microbes, associated with displayed longissimus lumborum was suppressed for muscle from vitamin E-supplemented steers. Taste panelists detected no difference among longissimus lumborum steaks from control and vitamin E-supplemented steers but found (P less than .01) steaks aged for 21 d to be more tender than steaks aged for 7 d. Supplementing cattle with vitamin E should reduce economic losses associated with discolored beef during retail display.

The effect of long-term feeding (252 days) of three supplemental levels of cx-tocopheryl acetate (actual 0, 360 and 1290 IU/head/day) on meat quality was evaluated in Holstein and beef breed steers. Tissue vitamin E concentrations were increased by each increment of supplementation. The color display life of fresh beef under simulated retail conditions was extended 2 to 5 days by vitamin E and lipid oxidation was markedly reduced. Microbial population was not affected by level of supplementation. No deterioration in sensory quality occurred for steaks from supplemented steers that were displayed until the time steaks from unsupplemented steers discolored.