J. Anim. Sci. 2004. 82:2092-2104
© 2004 American Society of Animal Science
Supplemental vitamin D3 concentration and biological type of steers. II. Tenderness, quality, and residues of beef1
J. L. Montgomery*,2,
M. B. King*,
J. G. Gentry
,
A. R. Barham*,
B. L. Barham*,
G. G. Hilton
,
J. R. Blanton, Jr.*,
R. L. Horst¶,
M. L. Galyean*,
K. J. Morrow, Jr.#,3,
D. B. Wester
and
M. F. Miller*,4
* Department of Animal and Food Science and
and
Department of Range, Wildlife, and Fisheries Management, Texas Tech University, Lubbock 79409;
and
School of Agribusiness and Agriscience, Middle Tennessee State University, Murfreesboro 37132;
and
Department of Agriculture, Angelo State University, San Angelo, TX 76909;
and
¶ National Animal Disease Center, USDA Agricultural Research Service, Ames, IA 50010; and
and
# Department of Cell Biology and Biochemistry, Texas Tech University Health Science Center, Lubbock, TX 79409
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Abstract
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Vitamin D3 was orally supplemented to determine the supplemental dose that improved beef tenderness in different cattle breed types. Feedlot steers (n = 142) were arranged in a 4 x 3 factorial arrangement consisting of four levels of supplemental vitamin D3 (0, 0.5, 1, and 5 million IU/steer daily) administered for eight consecutive days antemortem using three biological types (Bos indicus, Bos Taurus-Continental, and Bos Taurus-English). Warner-Bratzler shear force (WBSF) was measured at 3, 7, 10, 14, and 21 d postmortem, and trained sensory analysis was conducted at 7 d postmortem on LM, semimembranosus, gluteus medius, and supraspinatus steaks. Concentrations of vitamin D3 and the metabolites 25-hydroxyvitamin D3, and 1,25-dihydroxyvitamin D3 were determined in the LM, liver, kidney, and plasma. Biological type of cattle did not interact (P > 0.10) with vitamin D3 supplementation for sensory or tenderness traits, suggesting that feeding vitamin D3 for 8 d before slaughter affected the different biological types of cattle similarly. Supplementing steers with 0.5, 1, or 5 million IU/(steer(d) decreased (P < 0.05) LM WBSF at 7, 10, 14, and 21 d postmortem compared with controls, and vitamin D3 treatments of 0.5, 1, and 5 million IU decreased (P < 0.05) semimembranosus WBSF at 3, 7, and 14 d postmortem. In general, vitamin D3-induced improvements in WBSF were most consistent and intense in LM steaks. Sensory panel tenderness was improved (P < 0.05) by all vitamin D3 treatments in LM steaks. Sensory traits of juiciness, flavor, connective tissue, and off-flavor were not (P > 0.05) affected by vitamin D3 treatments. All vitamin D3 treatments decreased µ-calpain activity and increased muscle Ca concentrations (P < 0.05). Vitamin D3 concentrations were increased (P < 0.05) by supplementation in all tissues tested (liver, kidney, LM, and plasma); however, cooking steaks to 71°C decreased (P < 0.05) treatment residue effects. The vitamin D metabolite 1,25-dihydroxyvitamin D3 was increased (P < 0.05) only in plasma samples as a result of the vitamin D3 treatments. These results indicate that supplementation with vitamin D3 at 0.5 million IU/steer daily for eight consecutive days before slaughter improved tenderness in steaks from different subprimal cuts by affecting muscle Ca concentrations, µ-calpain activities, and muscle proteolysis, with only a small effect on tissue residues of vitamin D3.
Key Words: Beef • Biological-Type • Residues • Tenderness • Vitamin D
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Introduction
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Of the quality factors, juiciness, flavor, and tenderness, the later has been shown to be most variable and the most important sensory component affecting consumer satisfaction with beef (Savell et al., 1987
, 1989; Miller et al., 2001). Surveys of meat retailers and restaurateurs have indicated that beef tenderness varies greatly (Morgan et al., 1991; Hamby, 1992; Brooks et al., 2000), and the 1995 National Beef Quality Audit listed tenderness as a major beef quality problem and the second largest concern of the industry (Smith et al., 1995). Therefore, inadequate tenderness is costing the U.S. beef industry an estimated $200 to $300 million annually (Morgan, 1995; Smith et al., 1995; Miller et al., 2001).
One of the most effective ways of improving meat tenderness is postmortem aging. Myofibrillar proteolysis, as a result of the intracellular Ca2+-dependent proteases µ-calpain and m-calpain, has been shown to enhance meat tenderization (Koohmaraie et al., 1987; Edmunds et al., 1991). Injection of carcasses and meat cuts with CaCl2 has improved tenderness (Kerth et al., 1995; Miller et al., 1995; Wheeler et al., 1997) by accelerating postmortem proteolysis. Swanek et al. (1999) first reported that supplementation of vitamin D3 (VITD) improved beef LM tenderness; therefore, supplementation of VITD could act in a similar fashion in other Ca-induced tenderness improvement systems. Montgomery et al. (2002) reported supplementing at greater than 1 million IU of VITD/(steer•d) decreased feedlot performance and increased tissue residues of VITD. Before VITD supplementation can be implemented by the beef industry, the hurdles of tissue residue accumulation and negative feedlot performance must be overcome. To achieve this, the proper dose of VITD must be further defined. Our study was conducted to investigate the dose response of VITD feeding before slaughter on the tenderness of muscles from different biological types of cattle.
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Materials and Methods
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Experimental Design
The experimental design, treatments, and experimental animals were described in detail by Montgomery et al. (2004). One hundred fifty beef steers were purchased for use in this experiment. The steers were of three biological types consisting of Bos Taurus-English (n = 50), Bos Taurus-Continental (n = 50), and Bos indicus (n = 50). The lightest and heaviest steers of each biological type were not used in the experiment. The remaining 144 steers were split into the three respective breed types. Before the dietary treatment period began, two steers were removed from the experiment. The dietary treatments consisted of 0.0, 0.5, 1.0, or 5.0 million IU/steer of VITD (Roche Vitamins Inc., Nutley, NJ) administered daily during the last 8 d of feeding. Four pens of each biological type (three steers per pen) received one of the four vitamin D3 treatments for the last 8 d of a 123-d feeding trial.
Slaughter and Carcass Evaluation
After the 8-d vitamin D3 supplementation period, steers were transported the following morning to a USDA-inspected facility (Excel Corp., Plainview, TX) for slaughter. Blood was collected during exsanguination from each steer. Liver samples were collected from the right hepatic lobe (lobus hepatis dexter), and the remaining liver was discarded if the steer had been supplemented with vitamin D3. A 30-g LM sample was removed from each carcass at 20 min postmortem for calpain determination according to the procedures of Koohmaraie (1990). Following a 48-h spray chill (–1°C), carcasses were ribbed, and USDA quality and yield grade traits (USDA, 1997) were recorded, after which carcasses were fabricated according to Institutional Meat Purchase Specifications (IMPS; USDA, 1990). During fabrication, mock tenders (supraspinatus; IMPS #116b), strip loins (LM; IMPS #180), top butts (gluteus medius; IMPS #184), and inside rounds (semimembranosus; IMPS #168) were collected, vacuum-packaged, transported to the Texas Tech University Meat Laboratory, and stored at 2°C until further processed.
Warner-Bratzler Shear Force and Tenderness Determination
Each mock tender, strip loin, top butt, and inside round were further processed into individual supraspinatus, longissimus, gluteus medius, and semimembranosus muscles, respectively, 3 d postmortem. Each muscle was then cut into 2.54-cm-thick steaks, placed in Cryovac B160 beef bags, and wet-aged (in anerobic conditions) at 2°C. Steaks for each muscle were randomly allotted to an aging treatment of 3, 7, 10, 14, or 21 d postmortem for Warner-Bratzler shear force (WBSF) determinations, and aged for 7 d postmortem for sensory evaluations, as well as for chemical and water analyses. After the appropriate aging period, steaks were frozen at –20°C until further analyses.
Sensory panel evaluations and WBSF determinations were conducted according to AMSA (1995) guidelines. Steaks for sensory and WBSF determinations were thawed slowly in a 2°C cooler for 18 to 24 h, and cooked on a MagiGrill belt grill (model TBG-60 electric conveyor grill; MagiKitch’n, Quakertown, PA) for 5 min and 40 s with a grill-plate thickness of 2.16 cm and grill-plate temperature of 163°C to an internal steak temperature of 71°C. Individual steaks were weighed before and after cooking to determine cooking loss on WBSF steaks. Once cooked, steaks for WBSF evaluation were placed on plastic trays, covered with polyvinyl chloride film, and chilled for 18 to 24 h at 2°C. Five to six round, 1.27-cm-diameter cores were removed from each supraspinatus steak, six cores were removed from each LM steak, and eight cores were removed from each gluteus medius and semimembranosus steak parallel to the muscle fiber orientation, and sheared once with a WBSF machine (G-R Elec. Mfg. Co., Manhattan, KS). The multiple shear force determinations for each steak were then averaged for statistical analysis.
Sensory steaks were cut into 1-cm3 cubes immediately after cooking and stored in warming pans (approximately 5 min) until served (approximately 50°C) to the trained sensory panel (AMSA, 1995). Samples were evaluated by a six- to eight-member panel trained according to the standards of Cross et al. (1978). Steaks were evaluated for initial juiciness, sustained juiciness, initial tenderness, sustained tenderness, flavor intensity, beef flavor, overall mouth feel, and connective tissue (8 = extremely juicy, tender, intense, characteristic beef flavor, beef-like mouth feel, and none; 1 = extremely dry, tough, bland, uncharacteristic beef flavor, non-beef-like mouth feel, and abundant), as well as off flavor (5 = extremely off flavor; 1 = none).
Water-Holding Capacity and Chemical Analyses of Fresh Beef
Amount of purge was measured on individual strip loins, top butts, and inside rounds by weighing (to the nearest 0.01 g) individual cuts before removal from packaging and reweighing 10 min after removal. Drip loss was measured on LM (strip loin) and supraspinatus (mock tender) samples at 3 d postmortem by removing a 1.2-cm-diameter core from each muscle, placing the core in a drip loss tube (C. Chrestensen Laboratory, Denmark) and weighing the core sample before and after storage at 2°C for 24 h. Percentage of moisture, as well as percentages of free, bound, and immobilized water, were determined on LM samples using the procedures of Wierbicki and Deatherage (1958).
Muscle Ca and P concentrations were determined on LM samples according to AOAC (1990) techniques. A 5-g muscle sample was placed in a crucible and dried in a vacuum-drying oven at 100°C for 24 h. Samples were then ashed in a muffle furnace at 625°C for 18 h, cooled to room temperature, dissolved in 50 mL of 3 N HCl, and boiled down to a 25-mL volume. Samples were then filtered through Q2 filterpaper (Fisher Scientific, Houston, TX) into a 100-mL flask and diluted to 100 mL. Next, 4 mL of the diluted sample was placed in a test tube with 5.5 mL of distilled water and 0.5 mL of 5% (vol/vol) solution of lanthanum chloride. Calcium concentrations were determined in duplicate by atomic absorption spectrometry using standards of 0, 5, 10, and 15 mg of Ca2+/100 mL on a Perkin Elmer atomic absorption spectrometer (model 2380; Perkin Elmer Inc., Wellesley, MA). Muscle P concentrations were determined colorimetrically on the diluted samples in duplicate according to AOAC (1990) procedures using a Beckman DU-50 spectrophotometer (Beckman Coulter, Chaska, MN).
Vitamin D3, 25-Hydroxyvitamin D3, and 1,25-Dihydroxyvitamin D3 in Plasma, Beef, Liver, and Kidney
Vitamin D3, 25-hydroxyvitamin D3 (25-(OH)2 D3), and 1,25-dihydroxyvitamin D3 (1,25-(OH)2 D3) concentrations were determined by a modification of the methods outlined by Montgomery et al. (2000), as explained in Montgomery et al. (2002). For kidney, liver, muscle, and cooked steak (samples were cooked to 71°C and then stored at 4°C overnight) samples, 2 g of tissues was homogenized in 8 mL of PBS with a Polytron (Kinematica AG, Littan-Lucerne, Switzerland) for 60 s. A 2-mL aliquot of the homogenate was transferred to a 29- x 147-mm capped glass tube. Approximately 50 ng of vitamin D2 and 1,000 counts/min of 3H-25-(OH)2 D3 and 3H-1,25-(OH)2 D3 were added to the 2-mL aliquot for recovery estimates. Samples were then extracted, and the concentration of VITD was determined by HPLC using a Supelco Sil LC-5 column (0.46 x 25 cm) at 2 mL/min. Tissue concentrations of 25-hydroxyvitamin D3 and 1,25-(OH)2 D3 were determined after HPLC separation on a Supelco Sil LC-5 column (0.46 x 25 cm) followed by RIA. Plasma VITD, 25-(OH)2 D3, and 1,25-(OH)2 D3 concentrations also were determined using HPLC and RIA.
Troponin-T Degradation
Longissimus muscle samples were collected at 24 h postmortem and on d 7, 10, and 14 postmortem, and whole-muscle preparations were used to determine troponin-T degradation. For ease of collection and determination, a total of six animals was subsampled from each VITD treatment (n = 28 steers) for each of the aging periods. Samples were prepared as described by Huff-Lonergan et al. (1996b). A 7-d-aged sample from the control group was loaded on each 15% acrylamide SDS-PAGE gel to serve as an internal standard. Western blots were performed according to the method of Huff-Lonergan et al. (1996a) to detect the 30-kDa component, a proteolytic degradation product of troponin-T using Sigma antibody JLT-12 (Sigma, St. Louis, MO). The 30–kDa band was detected using a chemiluminescent signal with an Amersham detection kit (ECL #RPN 2106; Amersham Biosciences, Piscataway, NJ), and then quantified using a Kodak molecular analysis software package (Kodak, Tokyo, Japan).
Statistical Analyses
Tissue residues were analyzed using a 4 (vitamin D treatment) x 3 (biological type) factorial arrangement of treatments in a completely randomized design, where a pen of three steers was the experimental unit. For amounts of purge, drip loss, and sensory traits, a split-plot arrangement was used. The main plot was as described previously, whereas the subplot consisted of muscle type and all interactions; the error term for the main plot was vitamin D and biological type nested within pen and muscle, whereas the error term for the subplot was the residual error. For WBSF and cooking loss, a split-split-plot design was employed. The whole plot consisted of the factorial arrangement, the first subplot consisted of muscle effects and interactions, and the final subplot consisted of postmortem aging effects and aging interactions. The error term for the final subplot was the residual error. For all analyses, the experimental unit was a pen of steers, and an 
level of 5% was used. Data for the 4 x 3 factorial were analyzed according to Steel and Torrie (1980), least squares means were calculated using the GLM procedures of SAS (SAS Inst., Inc., Cary, NC), and treatment differences were determined using the PDIFF option. When data were analyzed as repeated measures (split-plot or split-split-plot design), the pooled standard errors were calculated according to Steel and Torrie (1980), means were calculated using the LSMEANS option, and means were separated by the LSD method. Critical differences were calculated for the LSD by calculating the Saiterthwaite df for the t-values (Saiterthwaite, 1946).
For troponin-T degradation analysis, the experimental unit was individual steer. Data were analyzed as a repeated-measures design. The main plot consisted of the four VITD treatments, and the error term used to detect main plot differences was VITD treatment nested with animal. The subplot consisted of postmortem aging time and the vitamin D x aging treatment interaction, and was tested using the error term for VITD nested within animal and aging treatments. The standard errors of the means and mean separation were performed as described previously for the split-plot designs.
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Results
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Muscle Biochemistry
Vitamin D3 treatments did not (P > 0.41) affect the percentage of purge for strip loins, top butts, or inside rounds. However, treating steers with 5 million IU/steer daily increased (P < 0.05) drip loss of both mock tender and strip loin steaks compared with all other levels of VITD (Table 1). Treating cattle with VITD did not affect (P > 0.05) LM moisture percent.
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Table 1. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on muscle drip loss, purge and moisture content, calpain activity, and calcium and phosphorus concentration
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The VITD treatments decreased (P < 0.05) µ-calpain activity in LM samples, whereas m-calpain activity was not (P > 0.05) affected by any VITD treatment (Table 1
). The concentrations of Ca and P in the LM are presented in Table 1. Longissimus muscle Ca was increased (P < 0.05) by all VITD treatments. Thus, VITD supplementation seemed to increase the Ca content of muscle thereby activating skeletal muscle µ-calpain and resulting in a decrease of µ-calpain activity when measured. There were no (P > 0.53) effects of VITD treatment on the P content of muscle. Carcass measurements indicated that all VITD treatments increased 24-h postmortem LM temperature and 3-h postmortem LM pH (Montgomery et al., 2004). Anaerobic glycolysis in muscle results in the production of lactate from glycogen reserves, causing a drop in muscle pH. A few hours after death, muscle pH typically drops from 7.2 to 5.5 (Penny, 1980). The overall relationship between the VITD treatments and effects on muscle temperature, pH, and drip loss are not fully clear and need further study.
Effects of VITD treatments on troponin-T degradation are presented in Table 2. Treating cattle with 5 million IU/(steer•d) of VITD increased (P < 0.05) the appearance of the 30-kDa degradation component of troponin-T in LM samples at d 1 and 14 postmortem. Treating steers with 1 million IU also increased (P < 0.05) troponin-T degradation at d 10 and 14 postmortem compared with controls (Table 2). Vitamin D supplementation had its greatest effects on increasing the 30-kDa component appearance on d 1 and 14 postmortem (Figure 1). Thus, the effects of VITD on LM Ca and µ-calpain activity correspond with degradation of troponin T, especially when the steers were treated with 5 million IU/(steer•d).
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Table 2. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on the amount of 30-kDa component in longissimus muscle samples after 1, 7, 10, and 14 d postmortem aginga
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Figure 1. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on troponin-T degradation. Western blots of LM samples (20 of µg of protein/lane) run on 15% SDS-PAGE gels and transferred to polyvinylidene difluoride (PVDF) membranes. The blots were incubated for 1 h at 25°C with monoclonal troponin-T antibody and detected using an enhanced chemiluminescent system. A) Samples from steers treated with 5 million IU of vitamin D3/(steer•d) for 8 d had greater (P < 0.05) troponin-T into the 30-kDa component than did controls at 1 d postmortem. B) Samples from steers treated with 1 and 5 million IU of vitamin D3/(steer•d) for 8 d had greater (P < 0.05) troponin-T degradation into the 30-kDa component than did controls 14 d postmortem.
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Warner-Bratzler Shear Force and Sensory Panel Evaluations
Vitamin D3 treatment effects on WBSF are shown in Table 3. Biological type and VITD did not interact for WBSF (P > 0.05); therefore, VITD treatments seemed to affect WBSF of different breeds equally. There was a VITD x muscle x aging treatment interaction (P = 0.04) for WBSF. Supplementing steers with 0.5, 1, or 5 million IU/(steer•d) decreased (P < 0.05) LM WBSF at 7, 10, 14, and 21 d postmortem compared with controls. Longissimus muscle WBSF at 3 d postmortem was also decreased (P < 0.05) by the 1 and 5 million IU VITD treatments. Vitamin D3 at 0.5, 1, and 5 million IU/(steer•d) decreased (P < 0.05) semimembranosus WBSF at 3, 7, and 14 d postmortem, and the 0.5 and 1 million IU VITD treatments decreased (P < 0.05) semimembranosus WBSF at 21 d postmortem. The 5 million IU/(steer•d) VITD treatment decreased (P < 0.05) semimembranosus WBSF at 10 d postmortem compared with controls.
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Table 3. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on Warner-Bratzler shear force values (vitamin D3 x muscle x aging treatment; P = 0.04)a
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Gluteus medius WBSF was decreased (P < 0.05) at 3 d postmortem when steers were fed 0.5 million IU/(steer•d), and 14-d-aged gluteus medius WBSF values were decreased (P < 0.05) when steers were fed 5 million IU/steer daily. By d 21 postmortem, there was no effect (P > 0.05) on WBSF values as a result of VITD treatment in gluteus medius steaks. Supraspinatus WBSF was not (P > 0.05) decreased by any VITD treatment on d 7, 10, 14, or 21 postmortem when compared with controls; however, WBSF was less (P < 0.05) at 3 d postmortem when steers were fed 0.5 million IU/steer daily. In general, improvements in WBSF as a result of VITD were largest in LM steaks. Vitamin D3 treatments decreased WBSF approximately 1 kg in LM steaks and 0.5 to 1 kg in semimembranosus steaks, whereas treatment effects in supraspinatus steaks were generally inconsistent. Of the VITD treatments tested, the 0.5 million IU of VITD/(steer•d) was the only treatment that improved WBSF in all four muscles tested.
Cooking loss differences are presented in Table 4. There was a VITD x muscle x aging treatment interaction (P = 0.05) for cooking loss; however, cooking loss differences were generally minor and of little practical importance. Treating steers with 5 million IU of VITD/d decreased (P < 0.05) cooking losses in the supraspinatus at 3 d postmortem, although this dose increased (P < 0.05) cooking losses at 14 d postmortem compared with controls. Of the four muscles tested for cooking loss, VITD treatments had the least affect on the LM.
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Table 4. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on cooking loss percent (vitamin D3 x muscle x aging treatment; P = 0.049).
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Vitamin D3 treatment effects on sensory panel traits are shown in Tables 5 and 6. The VITD and biological type did not interact (P > 0.06) for any sensory panel traits. Vitamin D3 treatment did not (P > 0.22) affect juiciness, connective tissue amount, beef flavor, flavor intensity, mouth feel, or off-flavor traits of the four muscles tested. Panel-evaluated sustained tenderness was increased by treating steers with 0.5 and 5 million IU of VITD/(steer•d) (P < 0.05; Tables 5 and 6). There was a VITD x muscle interaction (P = 0.01) for initial tenderness scores. All VITD treatments increased (P < 0.05) initial tenderness scores of LM samples, but only the 0.5 and 5 million IU levels of VITD increased initial tenderness scores of semimembranosus (P < 0.05; Table 5). Initial tenderness scores for gluteus medius and supraspinatus were not affected (P > 0.05) by any VITD treatment compared with controls (Table 6). Improvement of panel tenderness scores by VITD was consistent between LM and semimembranosus steaks, although semimembranosus (inside round) steaks were scored tougher (P < 0.05) than longissimus steaks.
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Table 5. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on sensory traits of longissimus muscle and semimembranosus steaks aged to 7 d postmortem
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Table 6. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on sensory traits of gluteus medius and supraspinatus steaks aged to 7 d postmortem
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Vitamin D Residues
Vitamin D3 is hydroxylated in the liver to 25-(OH)2 D3, and this intermediate metabolite is then hydroxylated to 1,25-(OH)2 D3 in the kidney. The effects of VITD supplementation on tissue residues are shown in Table 7. All VITD treatments increased (P < 0.05) vitamin D3 concentrations in kidney, LM, and plasma samples compared with controls. However, once muscle samples were cooked, there were no VITD treatment effects on VITD concentrations (P > 0.05). The 1 and 5 million IU VITD treatments increased (P < 0.05) VITD concentrations in liver samples compared with controls, whereas treating cattle with 5 million IU/(steer•d) resulted in a 75-, 33-, and 8-fold increase in liver, kidney, and LM vitamin D3 concentrations, respectively. Treating cattle with 1 million IU/steer of VITD resulted in the same trend on residues as with the 5 million IU/(steer•d) treatment, but to a lesser degree. However, once muscle samples were cooked, there were no (P > 0.05) VITD treatment effects on VITD concentrations in the LM. It is important to note that VITD and metabolite concentrations were greater in cooked LM samples than raw LM samples presumably as a result of moisture and cooking losses.
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Table 7. The effect of feeding vitamin D3 to feedlot steers for eight consecutive days before slaughter on vitamin D3, 25-hydroxyvitamin D3, and 1,25-dihydroxyvitamin D3 concentrations in liver, kidney, longissimus muscle, and plasma samples
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The 25-(OH)2 D3 concentrations in liver were increased (P < 0.05) by all VITD treatments compared with control samples (Table 7). Raw and cooked LM samples also had increased (P < 0.05) 25-(OH)2 D3 concentrations when steers were supplemented with 1 or 5 million IU of VITD/steer daily. Treating steers with 5 million IU of VITD/d increased (P < 0.05) 25-(OH)2 D3 residues in kidney samples compared with control kidney samples. There was a VITD x breed type interaction (P < 0.05) for plasma 25-(OH)2 D3 concentrations (Figure 2). The 1 and 5 million IU of VITD/(steer•d) treatments increased (P < 0.05) 25-(OH)2 D3 concentrations in plasma of Bos indicus and Bos Taurus-Continental cattle, whereas all VITD treatments increased (P < 0.05) 25-(OH)2 D3 concentrations in the plasma of Bos Taurus-English steers (Figure 2).
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Figure 2. The effect of biological type and feeding 0 (control), 0.5, 1, or 5 million IU of vitamin D3/(steer•d) to feedlot steers for eight consecutive days before slaughter on plasma 25-hydroxyvitamin D3 concentrations. Means with different letters within a biological type differ (P < 0.05).
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1,25-Dihydroxyvitamin D3 is the biologically active form of VITD that results in a number of physiological effects, including the upregulation of Ca-binding proteins. All VITD treatments increased (P < 0.05) 1,25-(OH)2 D3 concentrations in plasma samples, indicating the potential for biological effects (Table 7). However, 1,25-(OH)2 D3 concentrations in raw and cooked muscle and kidney were not (P > 0.34) affected by VITD treatment, but variation was high. Also, 1,25-(OH)2 D3 concentrations of liver samples did not (P > 0.05) differ as a result of VITD treatment compared with controls.
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Discussion
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Vitamin D3 has been classified as a secosteroid. In cattle, dietary (oral) VITD must be converted to its final metabolite, 1,25-(OH)2 D3, a process that takes approximately 3 to 5 d from initial treatment, which explains the delay of effect on blood Ca or DMI for approximately the first 5 d of supplementation. The longer cattle are supplemented, or the higher the dose, the greater the effect on Ca and DMI. Early studies with VITD in cattle indicated that supplementation at levels as low as 1 x 106 IU/d increased blood Ca and P, while decreasing the incidence of milk fever in dairy cows (Hibbs et al., 1946, 1951; Hibbs and Pounden, 1955); however, feeding as little as 2.5 x 105 IU/d of VITD for extended periods of time increased plasma concentrations of Ca (McDermott et al., 1985). In the current study, all the VITD treatments increased plasma Ca, and steers treated with 1 and 5 million IU of VITD/d had increased plasma P concentrations. The major function of the vitamin D in the body is to increase plasma concentrations of Ca. The three major target tissues of the steroid 1,25-(OH)2 D3 are the intestine, kidney, and bone. The mechanism by which 1,25-(OH)2 D3 functions is similar to that of other steroid hormones, with 1,25-(OH)2 D3 interacting stereo-specifically with an intracellular receptor protein. The steroid–receptor complex then associates with DNA in the nucleus of target cells, either to initiate the synthesis of specific RNA-encoded proteins that mediate a spectrum of biological responses (mainly Ca binding) or to mediate a selective repression of gene transcription (Reichel et al., 1989). There is increasing evidence to indicate that skeletal muscle is a target organ for vitamin D metabolites. First, the vitamin D receptor (VDR) is located in muscle, and gene activation increases the RNA synthesis of Ca-binding proteins (Boland and Boland, 1985; Costa et al., 1986). Also, 1,25-(OH)2 D3 rapidly (1 to 3 min after treatment) increases muscle intracellular Ca concentrations (Boland, 1986). The rapid actions of 1,25-(OH)2 D3 on skeletal muscle Ca uptake have been shown to result from modulation of the Ca channel through the cyclic adenosine monophosphate pathway (Boland and Boland, 1987; Vazquez et al., 1995).
Vitamin D3 supplementation increased muscle Ca and decreased µ-calpain activity in prerigor muscle samples at the time of sampling. Decreased µ-calpain activity measured at 20 min postmortem may be indicative of increased and active proteolysis in the live tissue before slaughter of the animals and collections of the samples for analyses. The calpains are cytosolic enzymes that degrade myofibrillar proteins at or near the Z-line of the muscle sarcomere, leading to postmortem tenderization of beef (Koohmaraie, 1992; Boehm et al., 1998). It seems that VITD supplementation increases muscle Ca and activates µ-calpain in the live muscle over the supplementation period, resulting in increased muscle degradation of troponin-T noted in the current study and previously (Montgomery et al., 2000). This increased protein degradation apparently led to improved shear force and sensory panel tenderness. Increased proteolysis, as a result of VITD treatment, could potentially explain increases in carcass temperature and pH and drip loss noted with added VITD (Montgomery et al., 2004). Vitamin D3 supplementation had its greatest effects on improving the tenderness of LM steaks, which is known as one of the most proteolytically active muscles in a carcass (Koohmaraie et al., 1988b; Ouali and Talmant, 1990; Kim et al., 1993). The lack of treatment effects on the tenderness of supraspinatus steaks can be most likely explained by the high amount of connective tissue found within this muscle (Rhee et al., 2004). The current study indicates that VITD could be very useful to the beef industry because it affects the entire carcass and muscles from all major primal cuts.
Because VITD and its metabolites are all fat-soluble substances that are deposited in tissues, they all pose potential toxicological hazards. Vitamin D3 supplementation increased VITD concentrations in muscle, kidney, and plasma samples, although cooking decreased differences in muscle. In particular, the 1 million and 5 million IU/(steer•d) treatments increased liver VITD residues. Because of the increased residues, as a result of supplementing cattle at a dose of 1 million IU/(steer•d) or higher for 8 d, producers should be discouraged from using this rate of supplementation. Montgomery et al. (2000, 2002) also noted that VITD supplementation dramatically increased tissue residues of VITD and its metabolites when a level of 5 million IU/d or higher was fed. Feeding 0.5 million IU/(steer•d) decreased VITD concentrations in the liver, which is of primary concern for the U.S. FDA. The current study is the first to indicate that kidneys should be eliminated from the food chain for all VITD-treated cattle because of potential toxicological hazards. These results indicate that livers pose a limited toxicological hazard when cattle were fed 0.5 million IU, although feeding 1 million IU/(steer•d) and higher doses dramatically increased the potential toxicological hazard in raw samples
High levels of VITD in the diet can be toxic to both cattle and humans. The RDA of VITD for a normal adult human is 200 IU/d, or 5 µg (NRC, 1989). At this rate, an adult would need to eat 110 g of steak (uncooked figures), 12 g of kidney, or 5 g of liver from steers treated with 5 million IU/d of VITD from the current study to meet their daily needs for this nutrient. Using values from our previous study (Montgomery et al., 2002), an adult would need to eat 67 g of steak or 9 g of liver from steers treated with 5 x 106 IU of VITD to meet their daily needs for VITD. Extrapolating, it would take as little as 88 g of cooked liver from VITD-treated cattle to deliver a potential toxic dose of VITD (Montgomery et al., 2002). Using consumption values of 300 g of muscle, 100 g of liver, and 50 g of kidney, as set by the FDA, to determine the toxicological hazard of compounds, liver residues would be 9.15, 19.6, and 99.6 µg of VITD for the 0.5, 1.0, and 5.0 million IU/(steer•d) treatments, respectively (FDA, 1994) At the NRC (1989) RDA levels, all VITD treatments would create the potential for excessive residues in liver and kidney, and the 1 and 5 million IU treatments would possibly result in high residues in raw muscle. Consumption of as little as 45 µg of VITD/d has been associated with signs of VITD toxicity in young children (AAP, 1963). At this rate (45 µg of VITD/d), it would take as little as 45 g of liver, or nearly 1 kg of LM, from cattle treated with 5 million IU/d to deliver a potentially toxic dose of VITD. Also, considering the FDA consumption values discussed above, all of the VITD treatments would have a safe VITD concentration in muscle and kidney; however, liver from the 5 million IU of VITD treatment group would be twice the concentration reported to be toxic in children (AAP, 1963; FDA, 1994). Another study found that the minimum dose required to cause toxicity was 1,250 µg/d of VITD (Miller and Hayes, 1982). At this level, none of the meat or liver samples in our study would pose a serious toxicological hazard.
It also should be noted that these possible toxicological hazards are expressed on a wet-tissue basis. Because cooking seemed to alter the concentrations of VITD and its metabolites, the potential tissue residue hazards may be further reduced by cooking. Assessment of toxicological hazards in tissues from VITD-treated cattle is further complicated by results suggesting that the RDA are grossly underestimated and should be increased to at least 250 µg/d for adults (Vieth, 1999). Because it is difficult to assess the toxicological hazards associated with VITD, determining the overall hazard of supplementing cattle with VITD is problematic. However, it is important to note that VITD supplementation at 5 million IU/(steer•d) is currently being commercially applied in the Republic of South Africa in cattle fed Zilmax (a beta agonist; Intervet, Millsboro, DE). Because meat is typically marketed within 14 d postmortem in the Republic of South Africa, and because Zilmax may increase carcass toughness, VITD supplementation is being used to alleviate any potential detrimental tenderness effects caused by feeding this ß-agonist (P. E. Strydom, Irene, Republic of South Africa, personal communication). Vitamin D3 supplementation seems to be working in improving beef tenderness in the Republic of South Africa, and to the author’s knowledge, no cases of human VITD toxicity have been reported.
Koohmaraie et al. (1988a) reported that carcasses infused with 0.3 M CaCl2 (10% of animal live weight) were more tender and reached their ultimate shear force values and maximum proteolysis within 24 h postmortem. This Ca infusion process is thought to fully activate the available calpains (Koohmaraie et al., 1989, 1990; Koohmaraie and Shackelford, 1991). The initial CaCl2 infusion studies led to a number of studies that demonstrated the effectiveness of CaCl2 injection of meat in activating the calpains and improving tenderness (Wheeler et al., 1993; Kerth et al., 1995; Lansdell et al., 1995). However, this technology has yet to be implemented by the meat industry because CaCl2 injection and/or infusion may result in off-flavor development (St. Angelo et al., 1991) and increased lean discoloration during retail conditions (Kerth et al., 1995), especially when concentrations injected were greater than 200 mM (Miller et al., 1995).
Vitamin D3 plays a vital role in maintaining blood concentrations of Ca and P (Schwartz, 1975; Horst, 1986; Hurwitz, 1996). The major effect of supplementing high levels of VITD is to increase Ca absorption in the gut and release of Ca from bone stores (Conrad and Hansard, 1957; Littledike and Goff, 1987). Feeding high levels of VITD (0.5 x 106 to 7.5 x 106) IU/(steer•d) for 4 to 10 d before slaughter has improved beef LM tenderness (Swanek et al., 1999; Montgomery et al., 2000, 2002). In these experiments, decreased Warner-Bratzler shear force was observed at 7 and 14 d postmortem, but not at 21 d postmortem. Montgomery et al. (2002) noted that VITD supplementation had its greatest effect on semimembranosus steaks compared with LM steaks, and suggested that feeding VITD would effectively improve tenderness in cattle that tend to produce tough beef but not in cattle that tend to produce tender beef. Karges et al. (1999) reported VITD supplementation for 4 or 6 d before slaughter decreased the WBSF force of LM and gluteus medius steaks at 14 and 21 d postmortem, whereas Vargas et al. (1999) fed steers different combinations of VITD and vitamin E, and reported that steaks from the steers fed VITD required less aging time than did control steaks to reach a WBSF of less than 3.86 kg (considered very tender in their laboratory).
The metabolite 1,25-(OH)2 D3 functions as other steroids (e.g., androgens and estrogens), and elicits its response in muscle through a receptor mechanism. Treating steers with 0.5 million IU/d increased plasma concentrations of Ca, and Ca within muscle, and activating calpain, which led to decreased calpain activity when measured at slaughter. Beef tenderness also was improved to some degree by this treatment in every muscle sampled. Several researchers have reported that VITD supplementation had minimal effects on tenderness, or failed to improve tenderness (Scanga et al., 2001; Reiling and Johnson, 2003; Foote et al., 2004), which suggests the need for further research and the possibility that VITD supplementation is only effective in animals that produce tough meat. It seems that VITD increases cytosolic Ca and activates the calpains in meat to accelerate postmortem tenderization (Swanek et al., 1999). The calpains also have been shown to be activated by VITD in carcinoma cell cultures (Ravid et al., 1994; Berry and Meckling-Gill, 1999). These results indicate that oral supplementation with VITD of 0.5 million IU/(steer•d) for eight consecutive days before slaughter improved WBSF in longissimus and semimembranosus steaks by affecting Ca metabolism and µ-calpain activity, but, more importantly, this dose resulted in much lower tissue residues and no adverse effects on feedlot performance (Montgomery et al., 2004) compared with doses of 1 and 5 million IU/(steer•d).
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Implications
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Vitamin D3 supplementation increased muscle Ca concentration, activated µ-calpain, increased degradation of the myofibrillar protein troponin-T, and improved beef tenderness of a variety of muscles within the carcass of beef steers. The improvement in tenderness of multiple muscles through the feeding of vitamin D3 8 d before slaughter provides the beef industry with a tool to improve the quality and consistency of beef at both the retail and food-service markets with little detrimental effect on feedlot performance traits, especially when a low dose (0.5 IU/steer daily) of vitamin D3 supplementation is employed. Supplementing steers at 1 million IU/steer or greater negatively affected feedlot performance and tissue residues. The improvement in shear force values noted in the longissimus, semimembranosus, and gluteus medius by 3 d postmortem indicates that vitamin D3 improved beef tenderness without the necessity of a lengthy aging process.
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Footnotes
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1 This research was funded in part by a grant from the National Cattlemen’s Beef Association, Texas Beef Council, Roche Vitamins, Inc., and the Center for Feed Industry Research and Education at Texas Tech University. Texas Tech University Publ. No. T-5-450. The authors are also grateful for help with the Western blots and SDS-PAGE gels from E. Huff-Lonergan, S. Lonergan, and the staff of Iowa State University. 
2 Current address: Intervet Inc., 29160 Intervet Lane, Millsboro, DE 19966.
3 Current address: Meridian Bioscience, Inc., 3471 River Hills Dr., Cincinnati, OH 45244.
4 Correspondence: Box 42162 (phone: 806-742-2804; fax: 806-742-0169; e-mail: mfmrraider{at}aol.com).
Received for publication October 6, 2003.
Accepted for publication April 7, 2004.
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Abstract
Introduction
