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Effects of Ractopamine in Combination with Various Hormone Implant Regimens on Growth and Carcass Attributes in Calf-Fed Holstein Steers
The Professional Animal Scientist 25 (2009):195–201
©2009 American Registry of Professional Animal Scientists
CRactopamine S : Effects of in Combination ASE
TUdY
with Various Hormone Implant Regimens on Growth and Carcass Attributes in Calf-Fed Holstein Steers P. D. Bass,* J. L. Beckett,† and R. J. Delmore Jr.†1 *Animal Science Department, Colorado State University, Fort Collins, CO 80523; and †Animal Science Department, California Polytechnic State University, San Luis Obispo 93407
ABSTRACT The β-adrenergic agonist ractopamine (RAC) was approved for use as a feed supplement for beef cattle to increase lean muscle deposition and improve feed efficiency. The effects of several anabolic hormone implants were examined with or without RAC to determine feedlot and carcass performance of calf-fed Holstein steers. Sixteen hundred cattle were evaluated in 2 phases; cattle were divided equally into 8 treatments: 1) a nonimplanted non-RAC-fed control; 2) implanted with 20 mg estradiol benzoate plus 200 mg progesterone (EP); 3) implanted with 24 mg estradiol plus 120 mg trenbolone acetate (HT); 4) implanted with 20 mg estradiol plus 80 mg trenbolone acetate (MT); 5) nonimplanted and administered 200 mg/d RAC in the feed (R); 6) implanted with EP and administered 200 mg/d RAC (EP+R); 7) implanted with HT and administered 200 mg/d RAC (HT+R); 8) implanted 1 Corresponding author: rdelmore@calpoly. edu
with MT and administered 200 mg/d RAC (MT+R). Cattle administered RAC in both studies had increased (P < 0.05) hot carcass weight (HCW) and LM area (LMA) over cattle not fed RAC. All RAC plus implant treatments in both phases had greater (P < 0.05) HCW and LMA than the control. In addition, HCW in nearly all treatments in both phases was greater than in the R treatment group (P < 0.05). Over both phases, LMA was increased with the implant plus RAC treatments over control treatments. Ultimately, the addition of RAC in feedlot diets of Holstein steers during the last 36 d on feed increased feed efficiency and carcass lean deposition in a manner that was additive to implant effects. Key words: hormone implant, β-agonist, ractopamine, Holstein steer, beef
INTRODUCTION Improving the efficiency of animal production and maximizing profitability are the main goals of feedlot
managers. Holstein steers have been observed to have rapid growth in addition to desirable marbling scores without excessive backfat (Garcia de Siles et al., 1977; Knapp et al., 1989; Perry et al., 1991). As a means of improving size of LM area (LMA) and lean deposition in the body, anabolic steroid hormone implants are routinely used. In addition, other means of improving lean deposition have been evaluated. Previous studies involving beef cattle have reported that the nutrient repartitioning agent, ractopamine-HCl (RAC), improves lean deposition as well as feed efficiency (Vogel et al., 2005; Sissom et al., 2007). Ractopamine, a β-adrenergic agonist, stimulates β-adrenoceptors on muscle cells, which in turn activates a series of responses resulting in phosphorylation of enzymes and regulatory factors important in metabolic regulation. These metabolic initiations increase protein synthesis, in addition to catabolism of lipids, which are then used for other metabolic processes (Moody et al., 2000).
196 Numerous studies have demonstrated the benefits of RAC on growth and red meat yield (Armstrong et al., 2004; Vogel et al., 2005; AvendanoReyes et al., 2006), yet few have examined the effects of RAC used in combination with anabolic hormone implants in cattle. There is also little information on the combined effect of both anabolic agents on calf-fed Holstein steers in feedlots. Therefore, the objective of this study was to feed RAC in combination with 4 different anabolic hormone regimens to calffed Holstein steers and determine the interactive effect on gain, lean deposition, and carcass quality.
MATERIALS AND METHODS Cattle Management Before the onset of the trial, at approximately 125 kg of BW, all steers received a 43.7-mg estradiol (E2) implant. Two groups of 800 Holstein steers each, averaging 442 kg and 12 to 14 mo of age, were weighed and allotted (100 animals per treatment) to 1 of 8 treatments: 1) nonimplanted non-RAC-fed control; 2) implanted with 20 mg estradiol benzoate plus 200 mg progesterone (EP); 3) implanted with 24 mg E2 plus 120 mg trenbolone acetate (TBA; HT); 4) implanted with 16 mg E2 plus 80 mg TBA (MT); 5) nonimplanted and administered 200 mg/d RAC in the feed (R); 6) implanted with EP and administered 200 mg/d RAC in the feed (EP+R); 7) implanted with HT and administered 200 mg/d RAC (HT+R) in the feed; 8) implanted with MT and administered 200 mg/d RAC (MT+R) in the feed. Phase-1 steers were implanted 104 d before harvest and phase-2 steers were implanted and fed 131 d before harvest. The 2 phases were used because of the limited number of resources for the study and harvest plant availability. Initial BW of the phase-1 steers were recorded before implantation and administered RAC 36 d before harvest. Phase-2 steers were implanted 131 d before harvest and administered RAC 36 d before harvest; no initial weights
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Table 1. Ration ingredients (% of DM) and nutrient composition1 Item Ingredient Corn, steam flaked Alfalfa Sudangrass hay Corn gluten feed Fat Urea Calcium carbonate Trace mineral + sodium Water, diluent Rumensin2 Vitamin A Vitamin E Ractopamine-HCl Total Composition DM, % NEm, Mcal/45.4 kg NEg, Mcal/45.4 kg CP, % Ether extract, % Ca, % P, %
Formulation 71.94 9.50 3.20 7.00 4.20 1.60 1.00 0.17 0.60 0.02 <0.01 0.01 0.02 100.00 84.38 105.92 73.51 12.59 9.43 0.65 0.30
All rations commercially formulated (Nutrition Laboratory Services, Phoenix, AZ).
1
Supplied by Elanco Animal Health (Greenfield, IN).
2
were recorded for phase-2 cattle. Steers were fed a corn- and alfalfabased ration (Table 1) for 104 or 131 d on trial, respectively. Steers were fed in a commercial feedlot in Yuma, Arizona. Feeding and ration mixing was conducted using a commercial mixing feed truck. Finish weights were determined from the hot carcass weight (HCW) by dividing HCW by an average dressing percentage of 61%. Average daily gain was assessed for cattle implanted for phase-1 cattle only. By the end of the feeding trial period, 10 head were excluded from the phase-1 group of cattle and 28 head were excluded from the phase-2 group of cattle because of illnesses. Steer was considered the experimental unit in this study.
Carcass Data Collection Steers were transported to a commercial harvest facility by truck, where they were kept separated according to treatment. Individual animal identity was maintained throughout the slaughter process. Hot carcass weights were recorded before the final rinse. Carcasses were chilled for 48 h at 2°C. The phase-1 group was evaluated for estimated percentage of KPH, skeletal maturity on a scale of 100 to 299 (100 to 199 = A, 200 to 299 = B), lean maturity on a scale of 100 to 299 (100 to 199 = A, 200 to 299 = B), marbling score on a scale of 400 to 999 (400 to 499 = Slight, 500 to 599 = Small, 600 to 699 = Modest, 700 to 799 = Moderate, 800 to 899 = Slightly Abundant, 900 to 999 = Moderately Abundant; AMSA, 2000), and adjusted fat thickness (FT), and both phases were assessed for LMA using a digital imaging camera (RMS Research, Fort Collins, CO). Carcass evaluations were conducted by experienced beef carcass evaluators.
Warner-Bratzler Shear Force Five top loin (longissimus lumborum) steaks (2.54 cm) were removed from 4 randomly chosen Choice and Select carcasses, vacuum packaged, aged for 14 d at 2 ± 1°C, and frozen and stored at −20°C before WarnerBratzler shear force analysis. Frozen steaks were thawed at 2 to 4°C for 24 h before cooking. Steaks were cooked on a flat electric grill (Hamilton Beach Portfolio Electric Grill, Model No. 31605AH, Hamilton Beach, Washington, NC) and heated to an internal temperature of 35°C before inverting. Once inverted, steaks were cooked to an internal temperature of 71°C, and were then removed from the heat and allowed to cool for 4 h to room temperature. All temperatures were recorded using a type K thermocouple (Accutuff 340, Cooper Atkins Corp., Gainesville, FL). Six cores, 1.27 cm in diameter, were removed from the cooled steaks. Cores were removed parallel to the longitudinal orientation of the muscle fibers using a handheld
197
Ractopamine effects on implanted Holstein steers
Table 2. Effects of ractopamine (RAC), implants, and combined implants + RAC on live animal and carcass characteristics of Holstein steers Steers fed 104 d Treatment1 RAC Non-RAC C EP MT HT R EP+R MT+R HT+R
Live finish wt, kg
Gain/head, kg
ADG, kg
136.6a 132.3a 118.8e 139.4cd 137.4cd 133.7cd 130.9d 132.2cd 142.8c 141.0cd
1.32a 1.27a 1.14e 1.34cd 1.32cd 1.28cd 1.26d 1.27cd 1.36c 1.36cd
587.8a 583.4a 569.8e 590.5cd 588.6cd 584.8cd 582.0d 583.3cd 594.0c 592.1cd
Steers fed 131 d HCW,2 kg
LMA, cm2
359.2a 356.1b 347.6e 360.4cd 359.3cd 357.3d 355.1d 356.0d 364.6c 361.2cd
74.8a 72.9b 69.0f 72.3e 75.5d 74.8d 71.6e 74.8d 78.1c 74.8d
HCW, kg 361.41a 355.72b 349.73f 359.17def 363.25de 350.6f 350.67f 372.51c 366.05cd 356.22ef
LMA, cm2 75.17a 73.62b 72.64d 74.19d 74.19d 73.44d 73.37d 75.01d 78.43c 73.89d
Means within a column with different superscripts differ (P < 0.05).
a–f
Eight treatments were evaluated: C = control; EP = 20 mg estradiol benzoate plus 200 mg progesterone implant; MT = 16 mg trenbolone acetate plus 80 mg estradiol implant; HT = 24 mg trenbolone acetate plus 120 mg estradiol implant; R = 200 mg/d RAC; EP+R = EP plus RAC, MT+R = MT plus RAC; HT+R = HT plus RAC.
1
2
HCW = hot carcass weight.
coring device. Cores not uniform in diameter, having obvious connective tissue defects, or otherwise not representative of the sample steak were not used for the study. Cores were sheared once perpendicularly to the longitudinal orientation of the muscle fiber using a Warner-Brazler shear force machine (G-R Manufacturing, Manhattan, KS) according to the method of Savell et al. (1994) and Boleman et al. (1997).
ences were identified between live finish weights of all cattle treated with and without RAC. Treatment MT+R had heavier (P < 0.05) finish weights than the control and R treatments.
All individual treatments, however, resulted in significantly greater (P < 0.05) finish weights than did the control treatment (Table 2). The finish weights as well as individual rela-
Statistical Analysis The experimental design of this study was a 2 × 4 factorial. Treatments were 2 RAC treatments and 4 anabolic hormone implant regimens. Response variables were analyzed by ANOVA using the GLM procedure (SAS Institute Inc., Cary, NC). Response variables were analyzed with initial BW as a covariate for cattle implanted 104 d only. In addition, HCW and LMA were further analyzed as combined for both phases to determine the interaction between RAC and implant treatments.
RESULTS AND DISCUSSION All results are expressed as least squares mean comparisons. No differ-
Figure 1. Effect of implant and implant with ractopamine on hot carcass weight (HCW) over both groups of animals (n = 1,562). Treatments included control (no implants), EP (20 mg estradiol benzoate plus 200 mg progesterone), MT (20 mg estradiol plus 80 mg trenbolone acetate), and HT (24 mg estradiol plus 120 mg trenbolone acetate). a–eDifferences in lettering among columns denote significance (P < 0.05).
198 tive BW gain per head of implanted cattle vs. nonimplanted cattle in this study are similar to those in previous studies (Thonney, 1987; Dawson et al., 1991; Mader et al., 1994; Foutz et al., 1997). The greater finish weights associated with the MT+R treatment, relative to cattle in the control and R treatments, were as expected. Improved finish weights have been demonstrated in cattle implanted with E2 compared with nonimplanted cattle or cattle given β-agonists alone (Dawson et al., 1991). The current trial demonstrated that individual treatments in which RAC was administered resulted in greater BW than the control treatment. No differences were reported between implanted treatments with vs. without RAC. No difference was found in ADG between cattle fed RAC and not fed RAC. All individual treatments had greater (P < 0.05) ADG than did the control treatment. In addition, the MT+R treatment resulted in greater (P < 0.05) ADG than treatment R (Table 2). There was no significant relative BW gain per head difference between cattle fed and not fed RAC (P > 0.05). All treatments demon-
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strated greater (P < 0.05) BW gain than the control treatment. Likewise, MT+R resulted in greater BW gain than treatment R (P < 0.05; Table 2). This study suggests no difference in ADG between the RAC and non-RAC main effect treatments. The lack of difference in ADG between cattle fed and not fed RAC in this study contradicts several other studies conducted previously using native beef cattle (Avendano-Reyes et al., 2006; Sissom et al., 2007). Alternatively, Quinn et al. (2008) did not see a difference in ADG between cattle fed and not fed RAC. Studies examining ADG with response to β-agonists have, for the most part, used native cattle. The Holstein breed, however, tends to grow in a dissimilar pattern compared with native cattle (Wegner et al., 2000). This information could help elucidate why the β-agonist RAC did not perform the same as in the earlier studies using native beef cattle (Avendano-Reyes et al, 2006; Sissom et al., 2007). However, one study involving Holstein steers fed RAC confirms the lack of difference in ADG observed in this study between cattle fed and not fed RAC (Vogel et al., 2005). Further
Figure 2. Effect of implant and implant with ractopamine on LM area (LMA) over both groups of animals (n = 1,562). Treatments included control (no implants), EP (20 mg estradiol benzoate plus 200 mg progesterone), MT (20 mg estradiol plus 80 mg trenbolone acetate), and HT (24 mg estradiol plus 120 mg trenbolone acetate). a–c Differences in lettering among columns denote significance (P < 0.05).
investigations are required to examine the effects of differing doses of RAC in response to ADG in Holstein calffed steers. Cumulatively, all cattle fed RAC had heavier HCW (P < 0.05) than cattle not fed RAC. In phase 1, MT+R had greater HCW (P < 0.05) than HT, EP+R, R, and the control. All treatments in phase 1 resulted in HCW greater than that of the control (P < 0.05; Table 2). Individual treatment groups from phase-2 cattle, however, differed from those in phase 1 in that cattle in the EP+R treatment finished with greater HCW (P < 0.05) than those in the EP, MT, HT, HT+R, R, and control treatments. In phase 2, cattle in the EP+R and MT+R treatments had greater HCW (P < 0.05) than those in the HT, HT+R, R, and control treatments. In phase 2, cattle in the MT treatment had greater HCW (P < 0.05) than those in the HT, R, and control treatments (Table 2). When both phases were analyzed together, the combined effects of implants and RAC demonstrated overall improvements in HCW over the control treatment, but not over all implanted treatments (Figure 1). In both phases, carcasses from cattle administered RAC resulted in heavier HCW compared with nonRAC-treated cattle. These data are similar to those observed in a study conducted with RAC-treated crossbred beef steers (Avendano-Reyes et al., 2006). The improved HCW of implanted cattle in both phases were expected because of the documented muscle deposition effects of anabolic steroids (Herschler et al., 1995; Foutz et al., 1997). The findings related to combination implant plus RAC treatments resulting in greater HCW than that of the control and R alone indicate potential growth benefits to combining the 2 growth-enhancement treatments. These 2 growth interventions elicit their effects through completely different mechanisms causing 2 separate anabolic actions occurring in a muscle cell (Granner, 2000; Moody et al., 2000). This dual action may potentially increase the gain even further than that of a steroid hormone
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Ractopamine effects on implanted Holstein steers
Table 3. Effects of ractopamine (RAC), implants, and combined implants + RAC on carcass characteristics of Holstein steers fed 104 d Treatment1 RAC Non-RAC C EP MT HT R EP+R MT+R HT+R
Estimated KPH, %
Skeletal maturity
Lean maturity
Marbling score
Adjusted fat thickness, cm
2.61a 2.66a 2.63d 2.66cd 2.62de 2.71cd 2.62de 2.69cd 2.53e 2.61de
136.0a 134.4a 123.8f 136.2e 141.9d 135.5e 125.5f 135.4e 149.0c 134.4e
139.0a 137.9a 125.7f 143.0d 151.0c 132.1e 131.3e 144.6d 149.6cd 130.6ef
554.1a 551.8a 579.8d 542.1e 520.9f 564.6d 619.2c 542.5e 518.8f 535.2ef
0.68a 0.69a 0.76c 0.69cde 0.63f 0.68def 0.72cd 0.67def 0.65ef 0.68def
Means within a column with different superscripts differ (P < 0.05).
a–f
Eight treatments were evaluated: C = control; EP = 20 mg estradiol benzoate plus 200 mg progesterone implant; MT = 16 mg trenbolone acetate plus 80 mg estradiol implant; HT = 24 mg trenbolone acetate plus 120 mg estradiol implant; R = 200 mg/d RAC; EP+R = EP plus RAC; MT+R = MT plus RAC; HT+R = HT plus RAC.
1
or β-agonists alone. No significant interactions were identified between implant and RAC when data were pooled from both phases for HCW. In both phases, cattle administered RAC resulted in greater LMA (P < 0.05) than non-RAC, as would be expected because of improved muscle deposition from the β-agonistic action (Miller et al., 1988; See et al., 2004; Gruber et al., 2007). In both phases, cattle treated with MT+R yielded larger average LMA (P < 0.05) than cattle in all other treatments. The relatively smaller size of the LMA compared with traditional beef breeds is a common concern regarding Holstein steers (Garcia de Siles et al., 1977; Knapp et al., 1989; Perry et al., 1991) and any method of increasing the size is desirable. When both phases were combined, treatment groups MT, HT, EP+R, and HT+R resulted in greater LMA (P < 0.05) than the EP, R, and control treatments. Treatments EP and R had greater LMA (P < 0.05) than the control treatment (Table 2). No difference was reported between any other individual treatment groups from the combined phases. Mean LMA in all implanted cattle was greater than (P < 0.05) in the nonimplanted cattle, which was expected from results of previous studies (Preston et al., 1995; Scheffler et al., 2003). When both phases were ana-
lyzed together, an interaction between RAC and implant treatment resulted (P = 0.04) for LMA, and the MT+R treatment resulted in a larger LMA than all other treatments. All other treatments had LMA larger than the control (Figure 2). It is interesting that the more moderate TBA and E2 implant treatment resulted in a larger LMA than the more aggressive implant using the same compounds. This occurrence may explain the interaction results observed with the implant and RAC, implying that the combination works well with the TBA plus E2 type implants at certain levels of steroid hormone. Further investigations are needed to determine the interaction between RAC and TBA plus E2 concerning LMA in the Holstein steer. Regardless of the interaction, there did appear to be an additive affect when RAC was combined with the steroid hormone implants EP and HT. The RAC vs. non-RAC treatments in phase 1 yielded no significant differences in skeletal maturity, indicating no increase in skeletal maturity caused by feeding RAC. Treatment group MT+R in phase 1 had the greatest (P < 0.05) skeletal maturity scores of all treatment groups. Treatment MT resulted in a greater (P < 0.05) skeletal maturity score than all other treatment groups except
MT+R. Treatments EP, HT, EP+R, and HT+R yielded greater (P < 0.05) skeletal maturity scores than the control and R treatments (Table 3). Differences in lean maturity scores between RAC and non-RAC treatments were not significant (P > 0.05). Treatment group MT yielded greater (P < 0.05) lean maturity scores than all other treatments. Groups EP, EP+R, and MT+R had greater (P < 0.05) lean maturity scores than the HT, HT+R, R, and control groups. Treatments HT and R had greater (P < 0.05) lean maturity scores than the control (Table 3). These data suggest that increased skeletal ossification as well as lean darkening may occur using the MT hormone treatment compared with other hormone implants. Increases in maturity scores may result in detrimental economic effects if the carcasses are seen as greater than A40 overall maturity (equivalent to a lean or skeletal score of 140), which can render them ineligible for export to certain countries (USDA, 1997). In previous studies, TBA and E2 implants have demonstrated increases in skeletal ossification when administered to beef cattle (Foutz et al., 1997; Roeber et al., 2000; Scheffler et al., 2003). It has also been proposed that exogenous sources of estrogen may hasten skeletal development (Foutz et al., 1997).
200 No differences in marbling scores were identified between RAC and non-RAC treatments. Cattle that were not implanted yielded greater (P < 0.05) marbling scores than those with implants. Carcasses from the R treatment group had significantly greater (P < 0.05) marbling scores than those in all other treatments, including the control group, an interesting and unexpected find. These data differ from previously published research that showed either a significant difference (Ricks et al., 1984) or no significant difference (Schiavetta et al., 1990) between the marbling score of control animals and those administered a β-agonist. Treatment groups HT and C resulted in mean marbling scores greater than those of groups EP, MT, EP+R, MT+R, and HT+R (P < 0.05). Groups EP and EP+R had greater marbling scores (P < 0.05) than those of groups MT and MT+R (Table 3). Marbling score results in this study are similar to those in previous work showing greater marbling scores of carcasses from nonimplanted vs. implanted cattle (Herschler et al., 1995). As predicted, cattle in the control treatment group produced carcasses with greater mean marbling scores than cattle in almost all other treatments when an implant only or an implant plus RAC was used. This is likely a result of the diversion of nutrients to lean rather than fat deposition by β-agonists (Moody et al., 2000; Armstrong et al., 2004) in addition to the dilution factor of the intramuscular fat as a result of the increased LMA (Duckett et al., 1999). No difference in FT was observed between RAC-treated and non-RACtreated cattle, possibly because of the tendency of the Holstein breed to deposit little in the way of 12thrib backfat (Garcia de Siles et al., 1977; Knapp et al., 1989; Perry et al., 1991), thereby minimizing any backfat that could have been observed. Carcasses from cattle in the control group had FT measurements greater (P < 0.05) than those in the MT, HT, EP+R, MT+R, and HT+R groups. Likewise, group R had FT
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measurements greater than groups MT and MT+R (P < 0.05; Table 3). Cattle treated with MT resulted in the lowest FT measurements (P < 0.05). These data can be explained by the detrimental effect on fat deposition generally seen in relation to hormone implants in beef cattle (Herschler et al., 1995). Treatment MT+R was found to have some of the smallest FT measurements, which coincide well with the low marbling scores observed. These results suggest that the growth potential of the MT+R cattle was not fully attained. The growth curve of these cattle may have been extended, leaving them in a transitional phase from muscle to fat deposition, as would be noted by the priority of tissue deposition stated by previous research (Bauman et al., 1982). Further investigations of implants and RAC involvement in fat deposition are required to determine the fat deposition trend with differing doses of RAC. No difference was reported for estimated percentage of KPH fat between cattle treated with RAC vs. those not treated with RAC, which is similar to previous research (Gruber et al., 2007). The HT, EP, EP+R, and control groups had significantly greater KPH fat percentages (P < 0.05) than the MT+R group (Table 3). It has been suggested that β-agonists have a tendency to decrease internal fat deposition (Moloney et al., 1990; Vogel et al., 2005). The same fat deposition-decreasing tendency has been observed for anabolic steroid hormone implants (Mader, 1994; Herschler et al., 1995). However, this was not the case in this study, which demonstrated that both aggressive hormone implant treatments (EP and HT) produced greater estimated KPH than the moderately aggressive implant (MT). In pursuing the estimated KPH deposition further, it was observed that many of the RAC plus implant groups revealed results similar to that of cattle in the control treatment. The reasons for these unexpected occurrences may be because of uncontrolled environmental effects,
and further investigations should be conducted. No differences were found between any RAC, implant, or individual treatment means regarding tenderness in the Warner-Bratzler shear force analysis. These results are somewhat unexpected because marbling scores, an indication of tenderness (Tatum, 1997), were affected by treatment.
IMPLICATIONS The study demonstrated the potential for Holstein steers to perform well with a RAC treatment in combination with certain anabolic steroid implants by improving ribeye area and HCW. Further research is needed to find optimal timing programs for the individual implant plus RAC treatments. The findings of the combination implant plus RAC treatments resulting in improved carcass weights and larger ribeye areas than the RAC or implant treatment alone, in some cases, indicate great potential in combining the growth enhancement treatments. The reduced marbling scores, which coincide with the improvements in overall animal growth, suggest this treatment combination may have extended the growth curve of these animals. The treated animals therefore require a longer period of time to achieve optimum muscle growth and fat deposition. The use of these implant plus β-agonist regimens shows potential in providing the beef industry with a more efficient Holstein steer for feedlots.
LITERATURE CITED AMSA. 2000. Meat Evaluation Handbook. Am. Meat Sci.Assoc., Savoy, IL. Armstrong, T. A., D. J. Ivers, J. R. Wagner, D. B. Anderson, W. C. Weldon, and E. P. Berg. 2004. The effect of dietary ractopamine concentration and duration of feeding on growth performance, carcass characteristics, and meat quality of finishing pigs. J. Anim. Sci. 82:3245. Avendano-Reyes, L., V. Tores-Rodriguez, F. J. Meraz-Murillo, C. Perez-Linares, F. Figueroa-Saavedra, and P. H. Robinson. 2006. Effects of two β-adrenergic agonists on finishing performance, carcass characteristics, and
Ractopamine effects on implanted Holstein steers meat quality of feedlot steers. J. Anim. Sci. 84:3259.
1989. Characterization of cattle types to meet specific beef targets. J. Anim. Sci. 67:2294.
Bauman, D. E., J. H. Eisemann, and W. B. Currie. 1982. Hormonal effects on partitioning of nutrients for tissue growth: Role of growth hormone and prolactin. Fed. Proc. 41:2538.
Mader, T. L. 1994. Effect of implant sequence and dose on feedlot cattle performance. J. Anim. Sci. 72:277.
Boleman, S. J., S. L. Boleman, R. K. Miller, J. F. Taylor, H. R. Cross, T. L. Wheeler, M. Koohmarie, S. D. Shakelford, M. F. Miller, R. L. West, D. D. Johnson, and J. W. Savell. 1997. Consumer evaluation of beef of known categories of tenderness. J. Anim. Sci. 75:1521. Dawson, J. M., P. J. Buttery, M. J. Lammiman, J. B. Soar, C. P. Essex, M. Gill, and D. E. Beever. 1991. Nutritional and endocrinological manipulation of lean deposition in forage-fed steers. Br. J. Nutr. 66:171. Duckett, S. K., D. G. Wagner, F. N. Owens, H. G. Dolezal, and D. R. Gill. 1999. Effect of anabolic implants on beef intramuscular lipid content. J. Anim. Sci. 77:1100. Foutz, C. P., H. P. Dolezal, T. L. Gardner, D. R. Gill, J. L. Hensley, and J. B. Morgan. 1997. Anabolic implant effects on steer performance, carcass traits, subprimal yields, and longissimus muscle properties. J. Anim. Sci. 75:1256. Garcia-de-Siles, J. L., J. H. Zeigler, L. L. Wilson, and J. D. Sink. 1977. Growth, carcass and muscle characters of Hereford and Holstein steers. J. Anim. Sci. 44:973. Granner, D. K. 2000. Hormone action. p. 534 in Harper’s Biochemistry. R. K. Murray, D. K. Granner, P. A. Mayes, V. W. Rodwell, ed. Appleton and Lange, Stamford, CT. Gruber, S. L., J. D. Tatum, T. E. Engle, M. A. Mitchell, S. B. Laudert, A. L. Schroeder, and W. J. Platter. 2007. Effects of ractopamine supplementation on growth performance and carcass characteristics of feedlot steers differing in biological type. J. Anim. Sci. 85:1809. Herschler, R. C., A. W. Olmstead, A. J. Edwards, R. L. Hale, T. Montgomery, R. L. Preston, S. J. Bartle, and J. J. Sheldon. 1995. Production responses to various doses and ratios of estradiol benzoate and trenbolone acetate implants in steers and heifers. J. Anim. Sci. 73:2873. Knapp, R. H., C. A. Terry, J. W. Savell, H. R. Cross, W. L. Mies, and J. W. Edwards.
Mader, T. L., J. M. Dahlquist, M. H. Sindt, R. A. Stock, and T. J. Klopfenstein. 1994. Effect of sequential implanting with Synovex on steer and heifer performance. J. Anim. Sci. 72:1095. Miller, M. F., D. K. Garcia, M. E. Coleman, P. A. Ekeren, D. K. Lunt, K. A. Wagner, M. Procknor, T. H. Welsh Jr., and S. B. Smith. 1988. Adipose tissue, longissimus muscle and anterior pituitary growth and function in clenbuterol-fed heifers. J. Anim. Sci. 66:12. Moloney, A. P., P. Allen, D. B. Ross, G. Olson, and E. M. Convey. 1990. Growth, feed efficiency and carcass composition of finishing Friesian steers fed the β-adrenergic agonist l-644,969. J. Anim. Sci. 68:1269. Moody, D. E., D. L. Hancock, and D. B. Anderson. 2000. Phenethanolamine repartitioning agents. p. 65 in Farm Animal Metabolism and Nutrition. J. P. F. D’Mello, ed. CABI Publishing, New York. Perry, T. C., D. G. Fox, and D. H. Beermann. 1991. Effect of an implant of trenbolone acetate and estradiol on growth, feed efficiency, and carcass composition of Holstein and beef steers. J. Anim. Sci. 69:4696. Preston, R. L., S. J. Bartle, T. R. Kasser, J. W. Day, J. J. Veenhuizen, and C. A. Baile. 1995. Comparative effectiveness of somatotropin and anabolic steroids in feedlot steers. J. Anim. Sci. 73:1038. Quinn, M. J., C. D. Reinhardt, E. R. Loe, B. E. Depenbusch, M. E. Corrigan, M. L. May, and J. S. Drouillard. 2008. The effects of ractopamine-hydrogen chloride (Optaflexx) on performance, carcass characteristics, and meat quality of finishing feedlot heifers. J. Anim. Sci. 86:902. Ricks, C. A., R. H. Dalrymple, P. K. Baker, and D. L. Ingle. 1984. Use of β-agonist to alter muscle and fat deposition in steers. J. Anim. Sci. 59:1247. Roeber, D. L., R. C. Cannell, K. E. Belk, R. K. Miller, J. D. Tatum, and G. C. Smith. 2000. Implant strategies during feeding: Impact on carcass grades and consumer acceptability. J. Anim. Sci. 78:1867. Savell, J., R. Miller, T. Wheeler, M. Khoohmaraie, S. Shackelford, B. Morgan, C. Calkins,
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M. Miller, M. Dikeman, F. McKeith, G. Dolezal, B. Henning, J. Busboon, R. West, F. Parrish, and S. Williams. 1994. Standardized Warner-Bratzler shear force procedures for genetic evaluation. http://savell-j.tamu.edu/ shearstand.html Accessed March 24, 2006. Scheffler, J. M., D. D. Buskirk, S. R. Rust, J. D. Cowley, and M. E. Doumit. 2003. Effect of repeated administration of combination trenbolone acetate and estradiol implants on growth, carcass traits, and beef quality of long-fed Holstein steers. J. Anim. Sci. 81:2395. Schiavetta, A. M., M. F. Miller, D. K. Lunt, S. K. Davis, and S. B. Smith. 1990. Adipose tissue cellularity and muscle growth in young steers fed the beta-adrenergic agonist clenbuterol for 50 days and after 78 days of withdrawal. J. Anim. Sci. 68:3614. See, M. T., T. A. Armstrong, and W. C. Weldon. 2004. Effect of a ractopamine feeding program on growth performance and carcass composition in finishing pigs. J. Anim. Sci. 82:2474. Sissom, E. K., C. D. Reinhardt, J. P. Hutcheson, W. T. Nichols, D. A. Yates, R. S. Swingle, and B. J. Johnson. 2007. Response to ractopamine-HCl in heifers is altered by implant strategy across days on feed. J. Anim. Sci. 85:2125. Tatum, D. 1997. National Cattlemen’s Beef Association Fact Sheet: Beef Grading. Series No. FS/MS005. National Cattlemen’s Beef Association, Centennial, CO. Thonney, M. L. 1987. Growth, feed efficiency and variation of individually fed Angus, Polled Hereford and Holstein steers. J. Anim. Sci. 65:1. USDA. 1997. United States Standards for Beef Carcasses. Livestock and Seed Program. Agricultural Marketing Service, Des Moines, IA. Vogel, G. J., A. A. Aguilar, A. L. Schroeder, W. J. Platter, S. B. Laudert, and M. T. Van Koevering. 2005. The effect of Optaflexx on growth performance and carcass traits of calffed Holstein steers fed to harvest. Optaflexx Exchange No. 5, AI9724. Elanco Animal Health, Greenfield, IN. Wegner, J., E. Albrecht, I. Fiedler, F. Teusher, H. J. Papstein, and K. Ender. 2000. Growth- and breed-related changes of muscle fiber characteristics in cattle. J. Anim. Sci. 78:1485.
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CRactopamine S : Effects of in Combination ASE
TUdY
with Various Hormone Implant Regimens on Growth and Carcass Attributes in Calf-Fed Holstein Steers P. D. Bass,* J. L. Beckett,† and R. J. Delmore Jr.†1 *Animal Science Department, Colorado State University, Fort Collins, CO 80523; and †Animal Science Department, California Polytechnic State University, San Luis Obispo 93407
ABSTRACT The β-adrenergic agonist ractopamine (RAC) was approved for use as a feed supplement for beef cattle to increase lean muscle deposition and improve feed efficiency. The effects of several anabolic hormone implants were examined with or without RAC to determine feedlot and carcass performance of calf-fed Holstein steers. Sixteen hundred cattle were evaluated in 2 phases; cattle were divided equally into 8 treatments: 1) a nonimplanted non-RAC-fed control; 2) implanted with 20 mg estradiol benzoate plus 200 mg progesterone (EP); 3) implanted with 24 mg estradiol plus 120 mg trenbolone acetate (HT); 4) implanted with 20 mg estradiol plus 80 mg trenbolone acetate (MT); 5) nonimplanted and administered 200 mg/d RAC in the feed (R); 6) implanted with EP and administered 200 mg/d RAC (EP+R); 7) implanted with HT and administered 200 mg/d RAC (HT+R); 8) implanted 1 Corresponding author: rdelmore@calpoly. edu
with MT and administered 200 mg/d RAC (MT+R). Cattle administered RAC in both studies had increased (P < 0.05) hot carcass weight (HCW) and LM area (LMA) over cattle not fed RAC. All RAC plus implant treatments in both phases had greater (P < 0.05) HCW and LMA than the control. In addition, HCW in nearly all treatments in both phases was greater than in the R treatment group (P < 0.05). Over both phases, LMA was increased with the implant plus RAC treatments over control treatments. Ultimately, the addition of RAC in feedlot diets of Holstein steers during the last 36 d on feed increased feed efficiency and carcass lean deposition in a manner that was additive to implant effects. Key words: hormone implant, β-agonist, ractopamine, Holstein steer, beef
INTRODUCTION Improving the efficiency of animal production and maximizing profitability are the main goals of feedlot
managers. Holstein steers have been observed to have rapid growth in addition to desirable marbling scores without excessive backfat (Garcia de Siles et al., 1977; Knapp et al., 1989; Perry et al., 1991). As a means of improving size of LM area (LMA) and lean deposition in the body, anabolic steroid hormone implants are routinely used. In addition, other means of improving lean deposition have been evaluated. Previous studies involving beef cattle have reported that the nutrient repartitioning agent, ractopamine-HCl (RAC), improves lean deposition as well as feed efficiency (Vogel et al., 2005; Sissom et al., 2007). Ractopamine, a β-adrenergic agonist, stimulates β-adrenoceptors on muscle cells, which in turn activates a series of responses resulting in phosphorylation of enzymes and regulatory factors important in metabolic regulation. These metabolic initiations increase protein synthesis, in addition to catabolism of lipids, which are then used for other metabolic processes (Moody et al., 2000).
196 Numerous studies have demonstrated the benefits of RAC on growth and red meat yield (Armstrong et al., 2004; Vogel et al., 2005; AvendanoReyes et al., 2006), yet few have examined the effects of RAC used in combination with anabolic hormone implants in cattle. There is also little information on the combined effect of both anabolic agents on calf-fed Holstein steers in feedlots. Therefore, the objective of this study was to feed RAC in combination with 4 different anabolic hormone regimens to calffed Holstein steers and determine the interactive effect on gain, lean deposition, and carcass quality.
MATERIALS AND METHODS Cattle Management Before the onset of the trial, at approximately 125 kg of BW, all steers received a 43.7-mg estradiol (E2) implant. Two groups of 800 Holstein steers each, averaging 442 kg and 12 to 14 mo of age, were weighed and allotted (100 animals per treatment) to 1 of 8 treatments: 1) nonimplanted non-RAC-fed control; 2) implanted with 20 mg estradiol benzoate plus 200 mg progesterone (EP); 3) implanted with 24 mg E2 plus 120 mg trenbolone acetate (TBA; HT); 4) implanted with 16 mg E2 plus 80 mg TBA (MT); 5) nonimplanted and administered 200 mg/d RAC in the feed (R); 6) implanted with EP and administered 200 mg/d RAC in the feed (EP+R); 7) implanted with HT and administered 200 mg/d RAC (HT+R) in the feed; 8) implanted with MT and administered 200 mg/d RAC (MT+R) in the feed. Phase-1 steers were implanted 104 d before harvest and phase-2 steers were implanted and fed 131 d before harvest. The 2 phases were used because of the limited number of resources for the study and harvest plant availability. Initial BW of the phase-1 steers were recorded before implantation and administered RAC 36 d before harvest. Phase-2 steers were implanted 131 d before harvest and administered RAC 36 d before harvest; no initial weights
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Table 1. Ration ingredients (% of DM) and nutrient composition1 Item Ingredient Corn, steam flaked Alfalfa Sudangrass hay Corn gluten feed Fat Urea Calcium carbonate Trace mineral + sodium Water, diluent Rumensin2 Vitamin A Vitamin E Ractopamine-HCl Total Composition DM, % NEm, Mcal/45.4 kg NEg, Mcal/45.4 kg CP, % Ether extract, % Ca, % P, %
Formulation 71.94 9.50 3.20 7.00 4.20 1.60 1.00 0.17 0.60 0.02 <0.01 0.01 0.02 100.00 84.38 105.92 73.51 12.59 9.43 0.65 0.30
All rations commercially formulated (Nutrition Laboratory Services, Phoenix, AZ).
1
Supplied by Elanco Animal Health (Greenfield, IN).
2
were recorded for phase-2 cattle. Steers were fed a corn- and alfalfabased ration (Table 1) for 104 or 131 d on trial, respectively. Steers were fed in a commercial feedlot in Yuma, Arizona. Feeding and ration mixing was conducted using a commercial mixing feed truck. Finish weights were determined from the hot carcass weight (HCW) by dividing HCW by an average dressing percentage of 61%. Average daily gain was assessed for cattle implanted for phase-1 cattle only. By the end of the feeding trial period, 10 head were excluded from the phase-1 group of cattle and 28 head were excluded from the phase-2 group of cattle because of illnesses. Steer was considered the experimental unit in this study.
Carcass Data Collection Steers were transported to a commercial harvest facility by truck, where they were kept separated according to treatment. Individual animal identity was maintained throughout the slaughter process. Hot carcass weights were recorded before the final rinse. Carcasses were chilled for 48 h at 2°C. The phase-1 group was evaluated for estimated percentage of KPH, skeletal maturity on a scale of 100 to 299 (100 to 199 = A, 200 to 299 = B), lean maturity on a scale of 100 to 299 (100 to 199 = A, 200 to 299 = B), marbling score on a scale of 400 to 999 (400 to 499 = Slight, 500 to 599 = Small, 600 to 699 = Modest, 700 to 799 = Moderate, 800 to 899 = Slightly Abundant, 900 to 999 = Moderately Abundant; AMSA, 2000), and adjusted fat thickness (FT), and both phases were assessed for LMA using a digital imaging camera (RMS Research, Fort Collins, CO). Carcass evaluations were conducted by experienced beef carcass evaluators.
Warner-Bratzler Shear Force Five top loin (longissimus lumborum) steaks (2.54 cm) were removed from 4 randomly chosen Choice and Select carcasses, vacuum packaged, aged for 14 d at 2 ± 1°C, and frozen and stored at −20°C before WarnerBratzler shear force analysis. Frozen steaks were thawed at 2 to 4°C for 24 h before cooking. Steaks were cooked on a flat electric grill (Hamilton Beach Portfolio Electric Grill, Model No. 31605AH, Hamilton Beach, Washington, NC) and heated to an internal temperature of 35°C before inverting. Once inverted, steaks were cooked to an internal temperature of 71°C, and were then removed from the heat and allowed to cool for 4 h to room temperature. All temperatures were recorded using a type K thermocouple (Accutuff 340, Cooper Atkins Corp., Gainesville, FL). Six cores, 1.27 cm in diameter, were removed from the cooled steaks. Cores were removed parallel to the longitudinal orientation of the muscle fibers using a handheld
197
Ractopamine effects on implanted Holstein steers
Table 2. Effects of ractopamine (RAC), implants, and combined implants + RAC on live animal and carcass characteristics of Holstein steers Steers fed 104 d Treatment1 RAC Non-RAC C EP MT HT R EP+R MT+R HT+R
Live finish wt, kg
Gain/head, kg
ADG, kg
136.6a 132.3a 118.8e 139.4cd 137.4cd 133.7cd 130.9d 132.2cd 142.8c 141.0cd
1.32a 1.27a 1.14e 1.34cd 1.32cd 1.28cd 1.26d 1.27cd 1.36c 1.36cd
587.8a 583.4a 569.8e 590.5cd 588.6cd 584.8cd 582.0d 583.3cd 594.0c 592.1cd
Steers fed 131 d HCW,2 kg
LMA, cm2
359.2a 356.1b 347.6e 360.4cd 359.3cd 357.3d 355.1d 356.0d 364.6c 361.2cd
74.8a 72.9b 69.0f 72.3e 75.5d 74.8d 71.6e 74.8d 78.1c 74.8d
HCW, kg 361.41a 355.72b 349.73f 359.17def 363.25de 350.6f 350.67f 372.51c 366.05cd 356.22ef
LMA, cm2 75.17a 73.62b 72.64d 74.19d 74.19d 73.44d 73.37d 75.01d 78.43c 73.89d
Means within a column with different superscripts differ (P < 0.05).
a–f
Eight treatments were evaluated: C = control; EP = 20 mg estradiol benzoate plus 200 mg progesterone implant; MT = 16 mg trenbolone acetate plus 80 mg estradiol implant; HT = 24 mg trenbolone acetate plus 120 mg estradiol implant; R = 200 mg/d RAC; EP+R = EP plus RAC, MT+R = MT plus RAC; HT+R = HT plus RAC.
1
2
HCW = hot carcass weight.
coring device. Cores not uniform in diameter, having obvious connective tissue defects, or otherwise not representative of the sample steak were not used for the study. Cores were sheared once perpendicularly to the longitudinal orientation of the muscle fiber using a Warner-Brazler shear force machine (G-R Manufacturing, Manhattan, KS) according to the method of Savell et al. (1994) and Boleman et al. (1997).
ences were identified between live finish weights of all cattle treated with and without RAC. Treatment MT+R had heavier (P < 0.05) finish weights than the control and R treatments.
All individual treatments, however, resulted in significantly greater (P < 0.05) finish weights than did the control treatment (Table 2). The finish weights as well as individual rela-
Statistical Analysis The experimental design of this study was a 2 × 4 factorial. Treatments were 2 RAC treatments and 4 anabolic hormone implant regimens. Response variables were analyzed by ANOVA using the GLM procedure (SAS Institute Inc., Cary, NC). Response variables were analyzed with initial BW as a covariate for cattle implanted 104 d only. In addition, HCW and LMA were further analyzed as combined for both phases to determine the interaction between RAC and implant treatments.
RESULTS AND DISCUSSION All results are expressed as least squares mean comparisons. No differ-
Figure 1. Effect of implant and implant with ractopamine on hot carcass weight (HCW) over both groups of animals (n = 1,562). Treatments included control (no implants), EP (20 mg estradiol benzoate plus 200 mg progesterone), MT (20 mg estradiol plus 80 mg trenbolone acetate), and HT (24 mg estradiol plus 120 mg trenbolone acetate). a–eDifferences in lettering among columns denote significance (P < 0.05).
198 tive BW gain per head of implanted cattle vs. nonimplanted cattle in this study are similar to those in previous studies (Thonney, 1987; Dawson et al., 1991; Mader et al., 1994; Foutz et al., 1997). The greater finish weights associated with the MT+R treatment, relative to cattle in the control and R treatments, were as expected. Improved finish weights have been demonstrated in cattle implanted with E2 compared with nonimplanted cattle or cattle given β-agonists alone (Dawson et al., 1991). The current trial demonstrated that individual treatments in which RAC was administered resulted in greater BW than the control treatment. No differences were reported between implanted treatments with vs. without RAC. No difference was found in ADG between cattle fed RAC and not fed RAC. All individual treatments had greater (P < 0.05) ADG than did the control treatment. In addition, the MT+R treatment resulted in greater (P < 0.05) ADG than treatment R (Table 2). There was no significant relative BW gain per head difference between cattle fed and not fed RAC (P > 0.05). All treatments demon-
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strated greater (P < 0.05) BW gain than the control treatment. Likewise, MT+R resulted in greater BW gain than treatment R (P < 0.05; Table 2). This study suggests no difference in ADG between the RAC and non-RAC main effect treatments. The lack of difference in ADG between cattle fed and not fed RAC in this study contradicts several other studies conducted previously using native beef cattle (Avendano-Reyes et al., 2006; Sissom et al., 2007). Alternatively, Quinn et al. (2008) did not see a difference in ADG between cattle fed and not fed RAC. Studies examining ADG with response to β-agonists have, for the most part, used native cattle. The Holstein breed, however, tends to grow in a dissimilar pattern compared with native cattle (Wegner et al., 2000). This information could help elucidate why the β-agonist RAC did not perform the same as in the earlier studies using native beef cattle (Avendano-Reyes et al, 2006; Sissom et al., 2007). However, one study involving Holstein steers fed RAC confirms the lack of difference in ADG observed in this study between cattle fed and not fed RAC (Vogel et al., 2005). Further
Figure 2. Effect of implant and implant with ractopamine on LM area (LMA) over both groups of animals (n = 1,562). Treatments included control (no implants), EP (20 mg estradiol benzoate plus 200 mg progesterone), MT (20 mg estradiol plus 80 mg trenbolone acetate), and HT (24 mg estradiol plus 120 mg trenbolone acetate). a–c Differences in lettering among columns denote significance (P < 0.05).
investigations are required to examine the effects of differing doses of RAC in response to ADG in Holstein calffed steers. Cumulatively, all cattle fed RAC had heavier HCW (P < 0.05) than cattle not fed RAC. In phase 1, MT+R had greater HCW (P < 0.05) than HT, EP+R, R, and the control. All treatments in phase 1 resulted in HCW greater than that of the control (P < 0.05; Table 2). Individual treatment groups from phase-2 cattle, however, differed from those in phase 1 in that cattle in the EP+R treatment finished with greater HCW (P < 0.05) than those in the EP, MT, HT, HT+R, R, and control treatments. In phase 2, cattle in the EP+R and MT+R treatments had greater HCW (P < 0.05) than those in the HT, HT+R, R, and control treatments. In phase 2, cattle in the MT treatment had greater HCW (P < 0.05) than those in the HT, R, and control treatments (Table 2). When both phases were analyzed together, the combined effects of implants and RAC demonstrated overall improvements in HCW over the control treatment, but not over all implanted treatments (Figure 1). In both phases, carcasses from cattle administered RAC resulted in heavier HCW compared with nonRAC-treated cattle. These data are similar to those observed in a study conducted with RAC-treated crossbred beef steers (Avendano-Reyes et al., 2006). The improved HCW of implanted cattle in both phases were expected because of the documented muscle deposition effects of anabolic steroids (Herschler et al., 1995; Foutz et al., 1997). The findings related to combination implant plus RAC treatments resulting in greater HCW than that of the control and R alone indicate potential growth benefits to combining the 2 growth-enhancement treatments. These 2 growth interventions elicit their effects through completely different mechanisms causing 2 separate anabolic actions occurring in a muscle cell (Granner, 2000; Moody et al., 2000). This dual action may potentially increase the gain even further than that of a steroid hormone
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Ractopamine effects on implanted Holstein steers
Table 3. Effects of ractopamine (RAC), implants, and combined implants + RAC on carcass characteristics of Holstein steers fed 104 d Treatment1 RAC Non-RAC C EP MT HT R EP+R MT+R HT+R
Estimated KPH, %
Skeletal maturity
Lean maturity
Marbling score
Adjusted fat thickness, cm
2.61a 2.66a 2.63d 2.66cd 2.62de 2.71cd 2.62de 2.69cd 2.53e 2.61de
136.0a 134.4a 123.8f 136.2e 141.9d 135.5e 125.5f 135.4e 149.0c 134.4e
139.0a 137.9a 125.7f 143.0d 151.0c 132.1e 131.3e 144.6d 149.6cd 130.6ef
554.1a 551.8a 579.8d 542.1e 520.9f 564.6d 619.2c 542.5e 518.8f 535.2ef
0.68a 0.69a 0.76c 0.69cde 0.63f 0.68def 0.72cd 0.67def 0.65ef 0.68def
Means within a column with different superscripts differ (P < 0.05).
a–f
Eight treatments were evaluated: C = control; EP = 20 mg estradiol benzoate plus 200 mg progesterone implant; MT = 16 mg trenbolone acetate plus 80 mg estradiol implant; HT = 24 mg trenbolone acetate plus 120 mg estradiol implant; R = 200 mg/d RAC; EP+R = EP plus RAC; MT+R = MT plus RAC; HT+R = HT plus RAC.
1
or β-agonists alone. No significant interactions were identified between implant and RAC when data were pooled from both phases for HCW. In both phases, cattle administered RAC resulted in greater LMA (P < 0.05) than non-RAC, as would be expected because of improved muscle deposition from the β-agonistic action (Miller et al., 1988; See et al., 2004; Gruber et al., 2007). In both phases, cattle treated with MT+R yielded larger average LMA (P < 0.05) than cattle in all other treatments. The relatively smaller size of the LMA compared with traditional beef breeds is a common concern regarding Holstein steers (Garcia de Siles et al., 1977; Knapp et al., 1989; Perry et al., 1991) and any method of increasing the size is desirable. When both phases were combined, treatment groups MT, HT, EP+R, and HT+R resulted in greater LMA (P < 0.05) than the EP, R, and control treatments. Treatments EP and R had greater LMA (P < 0.05) than the control treatment (Table 2). No difference was reported between any other individual treatment groups from the combined phases. Mean LMA in all implanted cattle was greater than (P < 0.05) in the nonimplanted cattle, which was expected from results of previous studies (Preston et al., 1995; Scheffler et al., 2003). When both phases were ana-
lyzed together, an interaction between RAC and implant treatment resulted (P = 0.04) for LMA, and the MT+R treatment resulted in a larger LMA than all other treatments. All other treatments had LMA larger than the control (Figure 2). It is interesting that the more moderate TBA and E2 implant treatment resulted in a larger LMA than the more aggressive implant using the same compounds. This occurrence may explain the interaction results observed with the implant and RAC, implying that the combination works well with the TBA plus E2 type implants at certain levels of steroid hormone. Further investigations are needed to determine the interaction between RAC and TBA plus E2 concerning LMA in the Holstein steer. Regardless of the interaction, there did appear to be an additive affect when RAC was combined with the steroid hormone implants EP and HT. The RAC vs. non-RAC treatments in phase 1 yielded no significant differences in skeletal maturity, indicating no increase in skeletal maturity caused by feeding RAC. Treatment group MT+R in phase 1 had the greatest (P < 0.05) skeletal maturity scores of all treatment groups. Treatment MT resulted in a greater (P < 0.05) skeletal maturity score than all other treatment groups except
MT+R. Treatments EP, HT, EP+R, and HT+R yielded greater (P < 0.05) skeletal maturity scores than the control and R treatments (Table 3). Differences in lean maturity scores between RAC and non-RAC treatments were not significant (P > 0.05). Treatment group MT yielded greater (P < 0.05) lean maturity scores than all other treatments. Groups EP, EP+R, and MT+R had greater (P < 0.05) lean maturity scores than the HT, HT+R, R, and control groups. Treatments HT and R had greater (P < 0.05) lean maturity scores than the control (Table 3). These data suggest that increased skeletal ossification as well as lean darkening may occur using the MT hormone treatment compared with other hormone implants. Increases in maturity scores may result in detrimental economic effects if the carcasses are seen as greater than A40 overall maturity (equivalent to a lean or skeletal score of 140), which can render them ineligible for export to certain countries (USDA, 1997). In previous studies, TBA and E2 implants have demonstrated increases in skeletal ossification when administered to beef cattle (Foutz et al., 1997; Roeber et al., 2000; Scheffler et al., 2003). It has also been proposed that exogenous sources of estrogen may hasten skeletal development (Foutz et al., 1997).
200 No differences in marbling scores were identified between RAC and non-RAC treatments. Cattle that were not implanted yielded greater (P < 0.05) marbling scores than those with implants. Carcasses from the R treatment group had significantly greater (P < 0.05) marbling scores than those in all other treatments, including the control group, an interesting and unexpected find. These data differ from previously published research that showed either a significant difference (Ricks et al., 1984) or no significant difference (Schiavetta et al., 1990) between the marbling score of control animals and those administered a β-agonist. Treatment groups HT and C resulted in mean marbling scores greater than those of groups EP, MT, EP+R, MT+R, and HT+R (P < 0.05). Groups EP and EP+R had greater marbling scores (P < 0.05) than those of groups MT and MT+R (Table 3). Marbling score results in this study are similar to those in previous work showing greater marbling scores of carcasses from nonimplanted vs. implanted cattle (Herschler et al., 1995). As predicted, cattle in the control treatment group produced carcasses with greater mean marbling scores than cattle in almost all other treatments when an implant only or an implant plus RAC was used. This is likely a result of the diversion of nutrients to lean rather than fat deposition by β-agonists (Moody et al., 2000; Armstrong et al., 2004) in addition to the dilution factor of the intramuscular fat as a result of the increased LMA (Duckett et al., 1999). No difference in FT was observed between RAC-treated and non-RACtreated cattle, possibly because of the tendency of the Holstein breed to deposit little in the way of 12thrib backfat (Garcia de Siles et al., 1977; Knapp et al., 1989; Perry et al., 1991), thereby minimizing any backfat that could have been observed. Carcasses from cattle in the control group had FT measurements greater (P < 0.05) than those in the MT, HT, EP+R, MT+R, and HT+R groups. Likewise, group R had FT
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measurements greater than groups MT and MT+R (P < 0.05; Table 3). Cattle treated with MT resulted in the lowest FT measurements (P < 0.05). These data can be explained by the detrimental effect on fat deposition generally seen in relation to hormone implants in beef cattle (Herschler et al., 1995). Treatment MT+R was found to have some of the smallest FT measurements, which coincide well with the low marbling scores observed. These results suggest that the growth potential of the MT+R cattle was not fully attained. The growth curve of these cattle may have been extended, leaving them in a transitional phase from muscle to fat deposition, as would be noted by the priority of tissue deposition stated by previous research (Bauman et al., 1982). Further investigations of implants and RAC involvement in fat deposition are required to determine the fat deposition trend with differing doses of RAC. No difference was reported for estimated percentage of KPH fat between cattle treated with RAC vs. those not treated with RAC, which is similar to previous research (Gruber et al., 2007). The HT, EP, EP+R, and control groups had significantly greater KPH fat percentages (P < 0.05) than the MT+R group (Table 3). It has been suggested that β-agonists have a tendency to decrease internal fat deposition (Moloney et al., 1990; Vogel et al., 2005). The same fat deposition-decreasing tendency has been observed for anabolic steroid hormone implants (Mader, 1994; Herschler et al., 1995). However, this was not the case in this study, which demonstrated that both aggressive hormone implant treatments (EP and HT) produced greater estimated KPH than the moderately aggressive implant (MT). In pursuing the estimated KPH deposition further, it was observed that many of the RAC plus implant groups revealed results similar to that of cattle in the control treatment. The reasons for these unexpected occurrences may be because of uncontrolled environmental effects,
and further investigations should be conducted. No differences were found between any RAC, implant, or individual treatment means regarding tenderness in the Warner-Bratzler shear force analysis. These results are somewhat unexpected because marbling scores, an indication of tenderness (Tatum, 1997), were affected by treatment.
IMPLICATIONS The study demonstrated the potential for Holstein steers to perform well with a RAC treatment in combination with certain anabolic steroid implants by improving ribeye area and HCW. Further research is needed to find optimal timing programs for the individual implant plus RAC treatments. The findings of the combination implant plus RAC treatments resulting in improved carcass weights and larger ribeye areas than the RAC or implant treatment alone, in some cases, indicate great potential in combining the growth enhancement treatments. The reduced marbling scores, which coincide with the improvements in overall animal growth, suggest this treatment combination may have extended the growth curve of these animals. The treated animals therefore require a longer period of time to achieve optimum muscle growth and fat deposition. The use of these implant plus β-agonist regimens shows potential in providing the beef industry with a more efficient Holstein steer for feedlots.
LITERATURE CITED AMSA. 2000. Meat Evaluation Handbook. Am. Meat Sci.Assoc., Savoy, IL. Armstrong, T. A., D. J. Ivers, J. R. Wagner, D. B. Anderson, W. C. Weldon, and E. P. Berg. 2004. The effect of dietary ractopamine concentration and duration of feeding on growth performance, carcass characteristics, and meat quality of finishing pigs. J. Anim. Sci. 82:3245. Avendano-Reyes, L., V. Tores-Rodriguez, F. J. Meraz-Murillo, C. Perez-Linares, F. Figueroa-Saavedra, and P. H. Robinson. 2006. Effects of two β-adrenergic agonists on finishing performance, carcass characteristics, and
Ractopamine effects on implanted Holstein steers meat quality of feedlot steers. J. Anim. Sci. 84:3259.
1989. Characterization of cattle types to meet specific beef targets. J. Anim. Sci. 67:2294.
Bauman, D. E., J. H. Eisemann, and W. B. Currie. 1982. Hormonal effects on partitioning of nutrients for tissue growth: Role of growth hormone and prolactin. Fed. Proc. 41:2538.
Mader, T. L. 1994. Effect of implant sequence and dose on feedlot cattle performance. J. Anim. Sci. 72:277.
Boleman, S. J., S. L. Boleman, R. K. Miller, J. F. Taylor, H. R. Cross, T. L. Wheeler, M. Koohmarie, S. D. Shakelford, M. F. Miller, R. L. West, D. D. Johnson, and J. W. Savell. 1997. Consumer evaluation of beef of known categories of tenderness. J. Anim. Sci. 75:1521. Dawson, J. M., P. J. Buttery, M. J. Lammiman, J. B. Soar, C. P. Essex, M. Gill, and D. E. Beever. 1991. Nutritional and endocrinological manipulation of lean deposition in forage-fed steers. Br. J. Nutr. 66:171. Duckett, S. K., D. G. Wagner, F. N. Owens, H. G. Dolezal, and D. R. Gill. 1999. Effect of anabolic implants on beef intramuscular lipid content. J. Anim. Sci. 77:1100. Foutz, C. P., H. P. Dolezal, T. L. Gardner, D. R. Gill, J. L. Hensley, and J. B. Morgan. 1997. Anabolic implant effects on steer performance, carcass traits, subprimal yields, and longissimus muscle properties. J. Anim. Sci. 75:1256. Garcia-de-Siles, J. L., J. H. Zeigler, L. L. Wilson, and J. D. Sink. 1977. Growth, carcass and muscle characters of Hereford and Holstein steers. J. Anim. Sci. 44:973. Granner, D. K. 2000. Hormone action. p. 534 in Harper’s Biochemistry. R. K. Murray, D. K. Granner, P. A. Mayes, V. W. Rodwell, ed. Appleton and Lange, Stamford, CT. Gruber, S. L., J. D. Tatum, T. E. Engle, M. A. Mitchell, S. B. Laudert, A. L. Schroeder, and W. J. Platter. 2007. Effects of ractopamine supplementation on growth performance and carcass characteristics of feedlot steers differing in biological type. J. Anim. Sci. 85:1809. Herschler, R. C., A. W. Olmstead, A. J. Edwards, R. L. Hale, T. Montgomery, R. L. Preston, S. J. Bartle, and J. J. Sheldon. 1995. Production responses to various doses and ratios of estradiol benzoate and trenbolone acetate implants in steers and heifers. J. Anim. Sci. 73:2873. Knapp, R. H., C. A. Terry, J. W. Savell, H. R. Cross, W. L. Mies, and J. W. Edwards.
Mader, T. L., J. M. Dahlquist, M. H. Sindt, R. A. Stock, and T. J. Klopfenstein. 1994. Effect of sequential implanting with Synovex on steer and heifer performance. J. Anim. Sci. 72:1095. Miller, M. F., D. K. Garcia, M. E. Coleman, P. A. Ekeren, D. K. Lunt, K. A. Wagner, M. Procknor, T. H. Welsh Jr., and S. B. Smith. 1988. Adipose tissue, longissimus muscle and anterior pituitary growth and function in clenbuterol-fed heifers. J. Anim. Sci. 66:12. Moloney, A. P., P. Allen, D. B. Ross, G. Olson, and E. M. Convey. 1990. Growth, feed efficiency and carcass composition of finishing Friesian steers fed the β-adrenergic agonist l-644,969. J. Anim. Sci. 68:1269. Moody, D. E., D. L. Hancock, and D. B. Anderson. 2000. Phenethanolamine repartitioning agents. p. 65 in Farm Animal Metabolism and Nutrition. J. P. F. D’Mello, ed. CABI Publishing, New York. Perry, T. C., D. G. Fox, and D. H. Beermann. 1991. Effect of an implant of trenbolone acetate and estradiol on growth, feed efficiency, and carcass composition of Holstein and beef steers. J. Anim. Sci. 69:4696. Preston, R. L., S. J. Bartle, T. R. Kasser, J. W. Day, J. J. Veenhuizen, and C. A. Baile. 1995. Comparative effectiveness of somatotropin and anabolic steroids in feedlot steers. J. Anim. Sci. 73:1038. Quinn, M. J., C. D. Reinhardt, E. R. Loe, B. E. Depenbusch, M. E. Corrigan, M. L. May, and J. S. Drouillard. 2008. The effects of ractopamine-hydrogen chloride (Optaflexx) on performance, carcass characteristics, and meat quality of finishing feedlot heifers. J. Anim. Sci. 86:902. Ricks, C. A., R. H. Dalrymple, P. K. Baker, and D. L. Ingle. 1984. Use of β-agonist to alter muscle and fat deposition in steers. J. Anim. Sci. 59:1247. Roeber, D. L., R. C. Cannell, K. E. Belk, R. K. Miller, J. D. Tatum, and G. C. Smith. 2000. Implant strategies during feeding: Impact on carcass grades and consumer acceptability. J. Anim. Sci. 78:1867. Savell, J., R. Miller, T. Wheeler, M. Khoohmaraie, S. Shackelford, B. Morgan, C. Calkins,
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M. Miller, M. Dikeman, F. McKeith, G. Dolezal, B. Henning, J. Busboon, R. West, F. Parrish, and S. Williams. 1994. Standardized Warner-Bratzler shear force procedures for genetic evaluation. http://savell-j.tamu.edu/ shearstand.html Accessed March 24, 2006. Scheffler, J. M., D. D. Buskirk, S. R. Rust, J. D. Cowley, and M. E. Doumit. 2003. Effect of repeated administration of combination trenbolone acetate and estradiol implants on growth, carcass traits, and beef quality of long-fed Holstein steers. J. Anim. Sci. 81:2395. Schiavetta, A. M., M. F. Miller, D. K. Lunt, S. K. Davis, and S. B. Smith. 1990. Adipose tissue cellularity and muscle growth in young steers fed the beta-adrenergic agonist clenbuterol for 50 days and after 78 days of withdrawal. J. Anim. Sci. 68:3614. See, M. T., T. A. Armstrong, and W. C. Weldon. 2004. Effect of a ractopamine feeding program on growth performance and carcass composition in finishing pigs. J. Anim. Sci. 82:2474. Sissom, E. K., C. D. Reinhardt, J. P. Hutcheson, W. T. Nichols, D. A. Yates, R. S. Swingle, and B. J. Johnson. 2007. Response to ractopamine-HCl in heifers is altered by implant strategy across days on feed. J. Anim. Sci. 85:2125. Tatum, D. 1997. National Cattlemen’s Beef Association Fact Sheet: Beef Grading. Series No. FS/MS005. National Cattlemen’s Beef Association, Centennial, CO. Thonney, M. L. 1987. Growth, feed efficiency and variation of individually fed Angus, Polled Hereford and Holstein steers. J. Anim. Sci. 65:1. USDA. 1997. United States Standards for Beef Carcasses. Livestock and Seed Program. Agricultural Marketing Service, Des Moines, IA. Vogel, G. J., A. A. Aguilar, A. L. Schroeder, W. J. Platter, S. B. Laudert, and M. T. Van Koevering. 2005. The effect of Optaflexx on growth performance and carcass traits of calffed Holstein steers fed to harvest. Optaflexx Exchange No. 5, AI9724. Elanco Animal Health, Greenfield, IN. Wegner, J., E. Albrecht, I. Fiedler, F. Teusher, H. J. Papstein, and K. Ender. 2000. Growth- and breed-related changes of muscle fiber characteristics in cattle. J. Anim. Sci. 78:1485.