Whey protein plus bicarbonate supplement has little effects on structural atrophy and proteolysis marker immunopatterns in skeletal muscle disuse during 21 days of bed rest.

OBJECTIVES: To investigate the effect of whey protein plus potassium bicarbonate supplement on disused skeletal muscle structure and proteolysis after bed rest (BR). METHODS: Soleus (SOL) and vastus lateralis (VL) biopsies were sampled from ten (n=10) healthy male subjects (aged 31±6 years) who did BR once with and once without protein supplement as a dietary countermeasure (cross-over study design). The structural changes (myofibre size and type distribution) were analysed by histological sections, and muscle protein breakdown indirectly via the proteolysis markers, calpain 1 and 3, calpastatin, MuRF1 and 2, both in muscle homogenates and by immunohistochemistry. RESULTS: BR caused size-changes in myofiber cross-sectional area (FCSA, SOL, p=0,004; VL, p=0.03), and myofiber slow-to-fast type transition with increased hybrids (SOL, p=0.043; VL, p=0.037) however with campaign differences in SOL (p<0.033). No significant effect of BR and supplement was found by any of the key proteolysis markers. CONCLUSIONS: Campaign differences in structural muscle adaptation may be an issue in cross-over design BR studies. The whey protein plus potassium bicarbonate supplement did not attenuate atrophy and fibre type transition during medium term bed rest. Alkaline whey protein supplements may however be beneficial as adjuncts to exercise countermeasures in disuse.

Influence of supplementing corn-soybean meal diets with vitamin E on performance and selected physiological traits of male turkeys.

Three experiments were conducted to determine the effects of supplementing practical diets of male turkeys with dl-alpha-tocopheryl acetate (TA). In Experiment 1, a factorial arrangement of dietary treatments [0, 12, 50, 150, and 300 IU TA/kg with 0 or 300 mg ascorbic acid (AA)/kg] was used. These 10 treatments were fed to poults from 1 to 41 d of age. From 41 to 118 d of age, the AA treatments were discontinued, and the 300 IU TA treatment groups were changed to 12 IU TA/kg. Neither TA nor AA treatments affected 41-d BW, feed to gain ratio (FE), or livability. No effects of dietary TA concentrations on turkey performance were observed through 118 d of age alpha-Tocopherol (TOC) concentrations of plasmas and livers were increased by increments of dietary TA, with substantial liver storage when toms were fed 150 IU TA/kg from 1 to 118 d. Supplementing diets with 0, 25, 50, 75, or 100 IU TA/ kg in Experiments 2 and 3 had no effect on performance of toms through 119 and 105 d, respectively. alpha-Tocopherol concentrations of plasma and red blood cells (RBC) increased linearly with increments of dietary TA. The same was true for livers in Experiment 2. Susceptibility of RBC to hemolysis induced by 400 microM t-butyl hydroperoxide (TBH) in Experiment 2 decreased with increasing dietary TA, and these decreases corresponded to increases in TOC concentration of RBC. However, the relationships between hemolysis and dietary TA or RBC TOC were inconsistent in Experiment 3 and varied according to concentration of TBH (200, 300, or 400 microM) and age of the toms. At 105 d of age, RBC of toms fed no supplemental TA were resistant to hemolysis, irrespective of dietary TA and TBH concentration. In Experiment 3, there were no indications of dietary TA effects on plasma peroxide concentration or activity of plasma creatine kinase. A positive relationship between dietary TA and blastogenic responses of blood lymphocytes was observed with concanavalin A when toms were at 44 d but not at 23 or 86 d of age. The overall data indicate that corn-soybean meal diets containing from 6 to 20 IU TOC/kg, but no supplemental TA supported satisfactory performance and well-being of male turkeys from 1 d of age to market ages when the turkeys were free of disease, as was true in the research reported here.

Efficacy of dietary and injected vitamin E for poults.

An experiment was conducted to compare the efficacy of two dietary sources and an injectable form of vitamin E (VE) to improve the VE status of poults. Six of the treatments consisted of a factorial arrangement of three concentrations and two sources of dietary VE. Turkeys in these treatments received 12, 80, or 150 IU of either dl-alpha-tocopheryl acetate or d-alpha-tocopherol (d-alpha-TOC)/kg of diet. The seventh treatment consisted of a single subcutaneous injection of d-alpha-TOC at 1 d of age. Poults in this treatment were subcutaneously injected in the dorsal area of the neck with 25 IU of d-alpha-TOC, this amount being approximately equivalent to the amount poults would consume if their diet was supplemented with 150 IU of VE/kg during their 1st wk of life. Concentration, source, or route of VE administration did not affect growth parameters, plasma creatine kinase, plasma triglycerides, or liver lipid peroxidation as measured by the thiobarbituric acid reactive substances assay (TBARS). Plasma, red blood cells (RBC), and liver alpha-TOC decreased from hatching to 14 d of age in poults fed either source of VE. The use of 80 or 150 IU of dietary VE (either source) reduced (P < 0.05) the extent of depletion of alpha-TOC at all ages and also reduced the susceptibility of RBC to hemolysis. There was no effect of source of dietary VE on concentration of alpha-TOC in plasma, RBC, or liver, or on RBC hemolysis. Subcutaneous injection of 25 IU of d-alpha-TOC at Day 1 increased (P < 0.05) alpha-TOC concentration until 7 d of age. Also, d-alpha-TOC injection reduced (P < 0.05) RBC susceptibility to hemolysis through 21 d of age. Data showed that one single subcutaneous injection of 25 IU of d-alpha-TOC at 1 d of age was as effective as 80 IU or more of dietary VE through 21 d to improve the alpha-TOC status of poults.

Influence of supplemental dietary fat on changes in vitamin E concentration in livers of poults.

An experiment was conducted to determine the influence of supplemental dietary fat on alpha-tocopherol (TOC) stored in the livers of young turkeys during the first 21 d after hatching. The four dietary treatments were obtained by supplementing a corn-soybean meal diet with 8% sucrose (SUC), 8% animal-vegetable fat (AVF), 8% tallow (TAL), or 8% coconut oil (COC). All diets were supplemented with 12 IU of dl-alpha-tocopheryl acetate (vitamin E)/kg of diet. Body weight at 21 d of age was not affected by dietary fat, whereas feed efficiency was improved (P < .05) by added fat, irrespective of source. Liver TOC (micrograms per gram of liver and micrograms per total liver weight) decreased markedly between 1 to 14 d of age, irrespective of fat source. Average TOC concentration in liver was 78.9 micrograms/g at 1 d, but was only .5 microgram/g at 14 d. Between 14 and 21 d of age, total liver TOC increased slightly in all treatment groups. No diet effect was observed on the liver TOC concentration until 21 d of age. At this time, poults fed TAL had less (P < .05) TOC in liver than those fed COC and AVF. The data show that neither the presence of supplemental dietary fat nor fat source changed the pattern of marked decrease in liver TOC during the first 14 d after hatching.

Research note: vitamin E status of turkey poults as influenced by different dietary vitamin E sources, a bile salt, and an antioxidant.

An experiment was conducted to determine the effects of level and chemical form of dietary vitamin E on alpha-tocopherol status of poults. The effects of a dietary bile salt and an antioxidant on concentrations of alpha-tocopherol in serum and liver were also tested. Six dietary treatments were obtained by supplementing a corn-soybean meal diet with 12 IU of DL-alpha-tocopheryl acetate (TA)/kg (LE), 12 IU of TA plus 800 mg of sodium taurocholate/kg (LB), 12 IU of TA plus 500 mg of ethoxyquin/kg (LS), 12 IU of D-alpha-tocopheryl polyethylene glycol 1,000 succinate (TPGS)/kg (LT), 100 IU of TA/kg (HE), and 100 IU of TPGS/kg (HT). Growth rate and feed efficiency of poults were unaffected (P > .05) by dietary treatments. The HE diet increased alpha-tocopherol in liver (P < .01) at 14 and 21 days of age. Liver and serum alpha-tocopherol concentrations were unaffected by dietary TPGS (LT and HT diets) at any age. Serum alpha-tocopherol concentration was unaffected by dietary treatments at 5 days of age. The HE diet, however, increased (P < .01) serum alpha-tocopherol at 9, 14, and 21 days of age. Age-related changes in alpha-tocopherol concentration were observed. Both liver and serum alpha-tocopherol decreased markedly from 1 to 14 days of age. The HE diet only partly alleviated the reduction of alpha-tocopherol in liver and serum. The water-soluble form of vitamin E, TPGS, dietary sodium taurocholate, or dietary ethoxyquin, did not prevent the marked decline in alpha-tocopherol concentration of liver and serum during the 21-day experiment.