Overview of the effects of beta-adrenergic receptor agonists on animal growth including mechanisms of action.

Several studies have shown that feeding of an energy-dense diet over short periods to cull cows could be profitable in terms of increased saleable yield and improved carcass conditions. Although the application of growth promoters, such as anabolic implants and beta agonists, in finishing of cull cows have been recorded, there is no conclusive evidence as to the timing and duration of beta agonists in cull cow production. In this study, 288 cull cows with four or more permanent incisors and varying weights and body conditions were divided into four treatment groups so that variation in age, weight and body condition were equally distributed among groups. One group received concentrate feed without any beta agonist (C), whereas the other three groups also received concentrate feed with zilpaterol hydrochloride (6 p.p.m.) for 20 (Z20), 30 (Z30) or 40 (Z40) days, respectively, followed by a 2-day withdrawal. Animals were adapted for 10 days on a grain-based diet and fed an additional 40 days before slaughter. Growth rate and efficiency (live and carcass), trimmed meat yield and meat tenderness (Warner Bratzler shear force and sensory) of the aged (10 days) m. longissimus thoracis (LT) and m. semitendinosus (ST) were recorded. In general, Z cows had higher carcass gains and efficiency of gain than C cows ( P , 0.05). In addition, Z carcasses showed higher proportional trimmed meat yields than C carcasses ( P , 0.05). No significant differences in tenderness measurements were recorded for LT or ST. In general, supplementation of zilpaterol for 30 days showed better growth performance and higher trimmed meat yield than 20 and 40 days supplementation.

Section: Discussionsupporting

confidence: 85%

Effects of duration of zilpaterol hydrochloride supplementation on growth performance, carcass traits and meat quality of grain-fed cull cows

Strydom

Smith

2010

“…From these data, we conclude that the loss of Mstn function increased muscularity and decreased adiposity as expected. Clenbuterol treatment, similar to several other bAA, improves feed efficiency, increases protein accretion, and therefore muscle mass, and decreases fat mass (Ricks et al, 1984, Yang andMcElligott, 1989;Mersmann, 1998;Beermann, 2002). As a selective b-2 agonist (Hinkle et al, 2002), clenbuterol likely alters protein degradation (Reeds et al, 1986;Yimlamai et al, 2005) to increase protein accretion, but may also alter protein synthetic rates.…”

Section: Discussionmentioning

confidence: 99%

“…The use of b-adrenergic agonists (bAA) to increase muscle mass and decrease fat mass in several species is well established (Ricks et al, 1984;Mersmann, 1998;Beermann, 2002). Clenbuterol, although not approved for commercial use in livestock, increases muscle growth in mice and other species (Yang and McElligott, 1989).…”

Section: Introductionmentioning

confidence: 99%

The myostatin null mutation and clenbuterol administration elicit additive effects in mice

Dilger

Gabriel

Kutzler

et al. 2010

In mice, the myostatin (Mstn) null mutation and treatment with clenbuterol both increase muscle growth and decrease fat mass. Our objective was to determine whether mechanistic overlap exists by administering clenbuterol to Mstn null mice. Male Mstn null and wild-type mice of similar genetic backgrounds received either 0 (control) or 20 p.p.m. clenbuterol in tap water free choice for 14 days. Several traits were measured to estimate muscle and fat growth. The Mstn null mutation resulted in increased body and empty carcass weight, increased muscle weights and decreased fat pad weights. Fat content was reduced and protein content was increased in the empty carcasses of Mstn null mice. Similarly, treatment with clenbuterol resulted in increased body and empty carcass weight, increased muscle weights and reduced fat pad weights. Fat content of empty carcasses and viscera was reduced and protein content of empty carcasses was increased with clenbuterol treatment. A significant interaction of genotype and clenbuterol treatment would indicate an altered responsiveness of Mstn null mice to clenbuterol. However, only the weight of gastrocnemius muscles exhibited a significant (P 5 0.01) interaction of genotype and clenbuterol treatment, indicating that Mstn null mice were less responsive to clenbuterol compared with wild-type mice. Thus, for all other traits, the impact of Mstn null mutation and clenbuterol treatment was completely additive. These data suggest that disruption of Mstn function does not alter the response of mice to b-adrenergic agonists.

“…b 2 -adrenergic receptor but not b1 adrenergic receptor is responsible for mediating the hypertrophic effect of clenbuterol (Hinkle et al, 2002). The growth promoting efficacy of b 2 -agonists appears to show animal species variation; ruminants display the greatest and broiler chickens the least response, with pigs occupying an intermediate position (Mersmann, 1998). Although the effects of b-agonists on meat quality are somewhat equivocal, the overall picture, in particular in the pig, is that many b-agonists decrease intramuscular fat and increase shear force or toughness (Dunshea et al, 2005).…”

Section: Fibre Size: Mediators Of Muscle Hypertrophy/atrophymentioning

confidence: 99%

Key signalling factors and pathways in the molecular determination of skeletal muscle phenotype

Chang

2007

The molecular basis and control of the biochemical and biophysical properties of skeletal muscle, regarded as muscle phenotype, are examined in terms of fibre number, fibre size and fibre types. A host of external factors or stimuli, such as ligand binding and contractile activity, are transduced in muscle into signalling pathways that lead to protein modifications and changes in gene expression which ultimately result in the establishment of the specified phenotype. In skeletal muscle, the key signalling cascades include the Ras-extracellular signal regulated kinase-mitogen activated protein kinase (Erk-MAPK), the phosphatidylinositol 3 0 -kinase (PI3K)-Akt1, p38 MAPK, and calcineurin pathways. The molecular effects of external factors on these pathways revealed complex interactions and functional overlap. A major challenge in the manipulation of muscle of farm animals lies in the identification of regulatory and target genes that could effect defined and desirable changes in muscle quality and quantity. To this end, recent advances in functional genomics that involve the use of micro-array technology and proteomics are increasingly breaking new ground in furthering our understanding of the molecular determinants of muscle phenotype.