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ANIMAL NUTRITION |
Department of Animal and Poultry Science, University of Guelph, Guelph, Ontario, Canada N1G 2W1
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Abstract |
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 Top Abstract INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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) and AA deficient (AA–; 40% below requirements; restriction phase). Thereafter (re-alimentation phase), pigs from both dietary AA levels were scale-fed or fed ad libitum diets that were not limiting in AA. Body weight gain and body composition, based on serial slaughter, were monitored during the 34-d re-alimentation phase. During the restriction phase AA intake restriction reduced BW gains (556 vs. 410 g/d; P < 0.001; AA+ and AA–, respectively). At 35 kg of BW, AA intake restriction increased whole body lipid content (11.1 vs. 17.5% of empty BW; P < 0.05) and the whole body lipid to body protein ratio (0.65 vs. 1.20; P < 0.01) and reduced body protein content (17.1 vs. 14.6% of empty BW; P < 0.01) and body water content (68.2 vs. 63.9%; P < 0.05). The relationships between body protein vs. body water and body protein vs. body ash content were not altered by previous AA intake restriction or by feeding level during the re-alimentation phase (P > 0.10). Throughout the re-alimentation phase, there were no interactive effects of time, feeding level, and previous AA intake level on growth performance, body protein, and body lipid content (P > 0.10). During the re-alimentation phase, body protein deposition, derived from the linear regression analysis of body protein content vs. time, was not affected by feeding level and previous AA intake level (P > 0.10; 156 g/d for AA– vs. 157 g/d for AA+). Based on BW and body protein content, it can be concluded that no compensatory body protein deposition occurred in barrows, with medium lean tissue growth potential after AA intake restriction between 15 and 35 kg of BW. It is suggested that the upper limit to body protein deposition was the main factor that limited the extent of compensatory body protein deposition in this population of pigs. The concept of an upper limit to body protein deposition may be used to explain why compensatory growth is observed in some studies and not in others.
Key Words: amino acid intake • body composition • compensatory growth • pig
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INTRODUCTION |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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; Kristensen et al., 2002; Reynolds and O’Doherty, 2006). As suggested by Kyriazakis and Emmans (1992), an understanding of the partitioning of DE and AA intake between body protein deposition (Pd) and body lipid deposition (Ld) may be required to predict the rate and extent of CG for individual groups of pigs. In growing pigs that are raised in a stress-free environment, Pd may be constrained by AA intake, the pigs’ genetically determined upper limit to body protein deposition (PdMax) or, during the energy dependent phase of Pd, energy intake over and above maintenance energy requirements and a minimum Ld to Pd ratio (minLd/Pd; De Greef, 1992). As discussed by De Greef (1992), there is a direct link between min-Ld/Pd and constraints on the whole body lipid (LB) to whole body protein ratio (PB; LB/PB). Constraints on LB/PB may be used to represent the effects of nutritional history on the composition of growth (Schinckel and de Lange, 1996), implying that Ld and Pd can be a reflection of the difference between actual and a pig genotype determined target LB/PB, as well as nutrient intake above maintenance nutrient requirements. The concepts of target LB/PB, rather than minLd/Pd, and PdMax may allow for the representation of compensatory Pd (CPd) after a period of AA restriction.
The objectives of this study were to investigate the dynamics of Pd and changes in body composition after AA intake restriction during the early grower phase in barrows with medium lean tissue growth potentials (PdMax approx 152 g/d; Möhn and de Lange, 1998). It was hypothesized that CPd only occurs during the energy dependent phase of Pd and is constrained by the pig’s PdMax and target LB/PB.
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MATERIALS AND METHODS |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The University of Guelph Animal Care Committee approved the experimental protocol.
Forty purebred Yorkshire barrows, from 18 different litters and weighing approximately 10 kg of BW, were obtained in 2 equal groups from the University of Guelph Arkell Swine Research Station herd and transported to the animal metabolism unit. The pigs were previously fed a commercial balanced pig starter diet ad libitum.
Upon arrival at the animal metabolism unit, pigs were housed individually in fully slatted floor pens (1 x 1.75 m) in an environmentally controlled room (22°C) and were given free access to water from nipple drinkers (Möhn and de Lange, 1998). Pigs were fed a pig starter diet ad libitum until the start of the experiment. From the start of the experiment, at approximately 15 kg of BW and when pigs were 6 to 7 wk old, pigs were fed equal amounts of feed twice daily at 0900 and 1600 h. Pigs were weighed weekly to monitor growth rate and to adjust feeding levels. Feed refusals were collected daily and weighed weekly to calculate actual feed intakes. Pigs were monitored twice daily for abnormal behavior and signs of disease.
Experimental Design and Diets
At 14.4 ± 1.6 kg of BW, pigs were randomly allotted to 1 of 2 dietary AA levels: deficient (AA–; n = 19 pigs) and adequate (AA+; n = 21 pigs) that were fed until pigs reached 35 kg of BW (restriction phase). During this phase, feed intake was restricted to 75% of the voluntary DE intake (DEi) according to NRC (1998):
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At this low level of energy intake, pigs were likely maintained within their energy-dependent phase of Pd up to 35 kg of BW (Möhn and de Lange, 1998). At 35 kg of BW, 8 pigs (4 pigs on AA– and AA+) were killed for determining physical and chemical body composition. At that time (d 0 of the re-alimentation phase) the remaining pigs were divided into 4 subgroups and fed the AA+ diet at 1 of 2 feed intake levels (ad libitum or restricted at 75% of voluntary DEi according to NRC, 1998), creating 4 treatments according to a 2 x 2 factorial arrangement:
Litter mates were assigned to different treatments. These pigs were killed at around d 14 (4 pigs per treatment; half of the pigs that were used for N-balance measurements) and d 34 of the re-alimentation phase (remaining pigs) for determining physical and chemical body composition. After the start of the re-alimentation phase, whole body N-balance was determined during 4 consecutive periods, using 16 pigs during periods I and II (4 pigs for each of the 4 treatments) and 8 pigs during periods III and IV (2 pigs for each of the 4 treatments) to monitor dynamics of Pd.
Diets used during the restriction phase contained AA levels that were either 40% below (0.60% standardized ileal digestible lysine; AA–) or 20% above estimated AA requirements (1.20% standardized ileal digestible lysine; AA+) for pigs between 5 and 10 kg of BW and with high lean tissue growth potentials (NRC, 1998). The profile of standardized ileal digestible essential AA was similar for AA+ and AA– and formulated based on the optimum dietary AA balance for starter pigs according to NRC (1998). The corn and soybean meal based diets were pelleted and formulated to ensure that intakes of vitamins, minerals, and essential fatty acids exceeded requirements according to NRC (1998; Table 1). Titanium oxide was added to the experimental diets as an indigestible marker for assessment of protein digestibility.
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Just before the end of the restriction phase and at approximately 32 kg of BW, 16 pigs were moved to adjustable metabolism crates for N-balance measurements (Möhn and de Lange, 1998). In these pigs, representing the 4 experimental treatments as outlined earlier, N-balance was monitored during 2 consecutive periods: period I, d 1 to 3, and period II, d 4 to 6. In half of these pigs, N-balances were monitored during another 2 consecutive periods: period III, d 13 to 18, and period IV, d 25 to 31. Between N-balance periods II, III, and IV, pigs were returned to the floor pens. Underneath the metabolism crates, 3 pans were placed for collection of wasted feed, urine, and feces, respectively. Feed refusals and wastage were collected quantitatively, pooled per pig for the entire N-balance period, dried, and weighed. The urine was collected quantitatively over 24-h periods in tared bottles containing 30 mL of 2 M sulphuric acid to keep pH below 3.0 for reducing ammonia loss. For every successful 24-h collection, urine was weighed and a 5% aliquot was taken, pooled per pig, and N-balance period in a sealable container and stored at 4°C. At the end of the N-balance period, the pooled aliquots were mixed thoroughly and 2 sub-samples were taken for N analysis. Uncontaminated feces were collected twice daily, pooled per pig and N-balance period, and stored at –20°C until processing.
Serial Slaughter Procedure
As outlined earlier, pigs were killed at either d 0 or approximately d 14 and 34 of the re-alimentation phase. The BW of the pigs was measured before electrical stunning and exsanguination according to Tuitoek et al. (1997) and Möhn and de Lange (1998). Blood was collected quantitatively, weighed, and discarded, whereas visceral organs (kidneys, spleen, liver, lungs, and heart) were weighed individually. The full gastrointestinal tract was weighed, emptied, and re-weighed to determine gut fill. Thereafter, the individual segments of the gastrointestinal tract (stomach, small and large intestine) were weighed. The empty gastrointestinal tract was added to the visceral organs and placed in a plastic bag and frozen at –20°C. The empty carcass (which included head, feet, hair, nails, and skin) was weighed, placed in plastic bags, and stored at –20°C as well.
Sample Preparation and Chemical Analysis
Pooled feces were thawed, weighed and homogenized in a Hobart mixer (Model C-100, Hobart Canada Inc., Delta, British Columbia, Canada). Two subsamples of approximately 250 g were taken from the mixed feces and weighed. One subsample was freeze-dried, whereas the other sample was stored at –20°C. Homogenization and sampling of carcass and viscera was performed according to Tuitoek et al. (1997). In short, pooled visceral organs and carcasses were removed from the freezer and weighed just before grinding. The carcasses and pooled visceral organs were ground separately for individual pigs using a large meat grinder (model B-801, Autio Company, Astoria, OR), 2 times using a 12.5-mm die and then once using a 6-mm die. After the last grinding, 2 homogeneous subsamples of approximately 400 g were taken from the carcass and pooled visceral organs, respectively. One subsample was weighed and freeze-dried, whereas the other sub-sample was weighed and stored at –20°C until nutrient analyses. Nutrients content of blood were taken from Weis et al. (2004).
The freeze-dried subsamples of carcass, pooled viscera, and feces were left for 24 h to equilibrate with room temperature and humidity and re-weighed to calculate water losses during freeze-drying. Freeze-dried samples (carcass, viscera, and feces) and samples of the 2 diets (AA+ and AA–) were ground with liquid N in a conventional coffee grinder. Duplicate samples were taken from each freeze-dried subsample to determinate analytical dry matter content according to AOAC (1997). Nitrogen content in samples of the diet, carcass, viscera, urine, and feces were determined in triplicate utilizing an induction furnace and thermal conductivity nitrogen gas analyzer (Leco FP-528, Leco Corporation, St. Joseph, MI). Ash content was determined in duplicate according to AOAC (1997). Fat content was determined in carcass, viscera, and feed by extraction of 2-g samples with ethyl-ether for 24 h without prior acid hydrolysis (AOAC, 1997). Freeze-dried feces and diet samples were analyzed for titanium dioxide content using standard procedures (AOAC, 1997). Diet AA contents were determined according to Llames and Fontaine (1994) in the laboratory of Degussa AG (Hanau, Germany).
Calculations and Statistical Analysis
All the calculations to determine body composition, Ld, Pd, and N retention are described in detail elsewhere (Möhn et al., 2000; Weis et al., 2004). Because of the low number of observations and small differences between subsequent slaughter BW, values for Pd and Ld were estimated from determined chemical body only across all 3 times of slaughtering pigs (approximately d 0, 14, and 32 of the re-alimentation phase) and using regression analyses.
The statistical analysis was performed using ANO-VA according to GLM procedure (SAS Inst. Inc., Cary, NC) in a complete randomized block design based on a 2 x 2 factorial arrangement (2 AA levels and 2 feed intake levels). Litter was first explored as a source of variation but was found not to be significant for the various response variables (P > 0.10) and removed from the statistical model. Initial BW was used as a covariate when growth performance was evaluated. Differences among treatment means were assessed using the Tukey honestly significant difference test. Regression analyses using GLM was conducted to evaluate linear and quadratic relationships between BW, PB, or LB and time, as well as the relationship between whole body ash content (AB) or whole body water content (WB) and PB. Probability levels less than P < 0.05 were considered significant, whereas 0.05 < P < 0.10 was considered a trend and P > 0.10 was considered not significant.
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RESULTS |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Unfortunately, 1 pig from treatment AA– (n = 19) was misplaced on treatment AA+ (n = 21). Generally, the pigs appeared in good health and no abnormalities in animal behavior were observed. However, during the restriction phase, 2 barrows on AA– were removed from the study due to illness and lack of appetite. The N balance data from 1 pig on AA+/Res (period 2) and another on AA–/Ad lib (periods 3 and 4) were excluded because of lack of appetite.
The analyzed CP content in the 2 experimental diets was as intended in the formulation (Table 1
). However, AA contents were 12% below anticipated levels. These systematic errors reflect an underestimation of nutrient contents in some of the ingredients or a systematic error in analytical procedures. This discrepancy does not influence the relative response to treatments.
Growth Performance
Initial BW did not differ between pigs on AA– and AA+ (P > 0.10). Between 15 and 35 kg of BW, pigs on AA– had a 26 and 28% lesser ADG and G:F, respectively, and consumed more feed as compared with pigs on AA+ (P < 0.001; Table 2).
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. During the first part of the re-alimentation phase (d 0 to 14), ad libitum fed pigs had greater ADG and ADFI (P < 0.001) than restricted fed pigs, whereas there were no differences (P > 0.10) in growth performance between pigs on AA+ and AA– (Table 3). Between d 14 and 34 of the re-alimentation phase, ad libitum fed pigs had greater ADFI and ADG and lesser feed efficiencies than restricted fed pigs (P < 0.02). Although pigs on AA– grew faster and had a greater feed efficiency between d 14 and 34 of the re-alimentation phase than pigs on AA+ (P < 0.05; Table 4), this effect was not apparent over the entire re-alimentation phase (Table 5). Over the entire re-alimentation phase and combined restriction and re-alimentation phases, ad libitum fed pigs had better growth performance than restricted fed pigs (P < 0.05; Table 5). Over the combined restriction and re-alimentation phases, pigs on AA– had lesser feed efficiencies than pigs on AA+, whereas pigs fed restricted had better feed efficiencies than pigs fed ad libitum (P < 0.05; Table 5).
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; P > 0.10). Whereas growth rates increased with feed intake level (P < 0.05), feed intake level did not affect the response to previous AA intake level (P > 0.10). At the final BW, pigs on AA– were 12 d older than pigs on AA+.
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After the restriction phase and at 35 kg of BW, there was no effect of dietary AA level on empty BW and weight of visceral organs (P > 0.10; data not shown), except for the weight of the kidneys, which was increased with AA intake (0.33 vs. 0.42% of empty BW, AA– and AA+, respectively; P < 0.05). Amino acid intake restriction tended to reduce the proportion of PB present in the carcass (86 vs. 85%; P = 0.083). At d 14 of the re-alimentation period, the weight of visceral organs was not affected by previous AA intake level (P > 0.10; data not shown), except for kidneys, which tended to be heavier in pigs on AA+ (0.44 vs. 0.47% of empty BW; P = 0.08). However, in ad libitum fed pigs, relative weights of liver (2.24 vs. 2.75% of empty BW; P < 0.01), kidneys (0.42 vs. 0.48% of empty BW; P < 0.01), and small intestine (2.1 vs. 2.75% of EBW; P = 0.051) were greater than in pigs fed restricted AA levels. Also, the distribution of PB between the viscera (10 vs. 12%; P < 0.05) and carcass (86 vs. 84%; P < 0.05) fractions was affected by energy intake (Res vs. Ad lib, respectively). The latter was consistent with the effect of energy intake level on the contribution of carcass weight to EBW (85 vs. 83%; P < 0.001). At d 34 of the re-alimentation phase, only the weight of kidneys was greater in ad libitum fed pigs (0.35 vs. 0.39% of empty BW; P < 0.001). At final slaughter BW, there were interactive effects of feeding level and diet AA level on spleen weight (P < 0.05). In pigs receiving AA+, spleen weight was greater in restricted fed pigs than in ad libitum fed pigs (0.17 vs. 0.13% of empty BW; P < 0.05), whereas in pigs on AA–, feeding level did not influence spleen weights (P > 0.10). The distribution of PB between viscera and carcass fractions as well as the contribution of carcass weight to EBW was not affected by either feeding level or AA intake (P > 0.10; data not shown).
Chemical Body Composition
At 35 kg of BW, dietary AA intake restriction increased LB (11.1 vs. 17.5% of empty BW; P < 0.02) and the LB/PB ratio (0.65 vs. 1.15; P < 0.005) and reduced PB (17.1 vs. 14.6% of empty BW; P < 0.002) and WB (68.2 vs. 63.9% of empty BW; P < 0.03; Table 2). Dietary AA level did not affect the relationships among AB, WB, and PB or the relationships among carcass protein content, viscera protein content, and PB (P > 0.10; data not shown).
At d 14 of the re-alimentation period, there were interactive effects of feeding level and diet AA level during the restriction phase on LB and LB/PB (P < 0.02; Table 3). In pigs on AA–, LB and LB/PB were numerically greater in restricted fed pigs than ad libitum fed pigs, whereas in pigs receiving AA+, LB and LB/PB were numerically greater in ad libitum fed pigs than restricted fed pigs. Moreover, previous AA intake level had an effect on PB, LB, LB/PB, and WB (P < 0.01) consistent with body composition at 35 kg of BW. In pigs fed ad libitum, the proportion of PB present in viscera and carcass was greater and lesser, respectively, than in pigs fed restricted (P < 0.05). At the final BW on d 34 of the re-alimentation phase, interactive effects on PB, LB, and LB/PB were observed (P < 0.05). In ad libitum fed pigs, differences in chemical body composition, observed at d 0 and d 14 of the re-alimentation phase, were no longer present, whereas in the restricted fed pigs group, pigs on AA– still had greater LB/PB, LB, and lesser PB than pigs on AA+.
Linear regression analysis showed no effects (P > 0.10) of feeding level and dietary AA level during the restriction phase on the relationship between carcass protein content and PB, viscera protein content and PB, AB and PB, WB and PB0.855, and lipid carcass content and LB (data not shown).
Body Protein Deposition and Body Lipid Deposition
For each of the 4 treatment combinations, the relationship between PB or LB and the time during the re-alimentation phase was linear (P < 0.05) and not quadratic (P > 0.10). The slopes of these relationships, representing Pd and Ld, were not affected (P > 0.10) by dietary AA level during the restriction phase, indicating that no CPd was observed after AA intake restriction. However, in ad libitum fed pigs, the numerically greater Ld for pigs on AA+ compared with AA– (294 and 248 g/d, respectively) contributed to an increase in LB/PB with BW that was not observed in restricted-fed pigs. During the re-alimentation phase, Ld (P < 0.05), but not Pd (P > 0.10), was increased with feeding level. Based on the serial slaughter data and across the 2 feeding levels, Pd in pigs on AA+ and AA– was 156 ± 1 and 157 ± 1 g/d, respectively (Figure 2).
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There was no interactive effect (P > 0.10) of feeding level and previous diet AA level on Pd during the 4 N-balance periods during the re-alimentation phase (Table 6). Given the small number of N-balance observations per treatment, results are presented separately for each of the 2 main effects (Table 6). Although AA intake did not affect (P > 0.10) Pd during the subsequent re-alimentation phase, Pd was numerically greater in pigs on AA– than AA+ during the third and fourth N-balance period. Furthermore, Pd increased (P < 0.05) with feed intake level during the first 2 periods of the re-alimentation phase (P < 0.05). Lysine utilization was not affected by previous diet AA level and feeding level during the re-alimentation phase (P > 0.10).
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DISCUSSION |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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During the restriction phase, pigs on AA– had a considerably poorer growth performance than those on AA+. Similar results have been observed in other studies (Zimmerman and Khajarern, 1973; Wahlstrom and Libal, 1983; Kyriazakis et al., 1991; Chiba, 1994, 1995; Critser et al., 1995; Whang et al., 2003). As expected, the restriction of AA intake between 15 and 35 kg of BW generated pigs with fatter carcasses as compared with pigs fed diets not limiting in AA content. The composition of growth (Ld/Pd) was altered by nutrition, generating differences in body composition (LB/PB) between dietary treatments at the end of the restriction phase. De Greef et al. (1992), Ferguson and Theeruth (2002), and Whang et al. (2003) reported similar results. The effort to create clear nutritionally induced differences in body fatness of pigs at 35 kg of BW was, therefore, successful.
Little consideration has been given to the impact of previous nutrition on the relationships between AB, WB, and PB. Kyriazakis et al. (1991) reported that pigs fed protein limiting diets had significant greater ratios of A/PB and W/PB0.855 as compared with control pigs, whereas these differences disappeared during the re-alimentation phase. In contrast to Kyriazakis et al. (1991), in the current study no significant treatment effects were observed on these ratios (P > 0.10). De Lange et al. (2003) suggested that most of the variations in chemical body composition, among different groups of pigs, can be attributed to the variation in LB and LB/PB, which is confirmed by the findings in this study.
Growth Performance During the Re-alimentation Phase
Many experiments have demonstrated that after a period of protein intake restriction, pigs are able to exhibit CG (Chiba, 1994, 1995; Critser et al., 1995; Fabian et al., 2002). However, in this current experiment dietary AA level during the restriction phase did not affect growth performance during the re-alimentation phase. Chiba et al. (1999, 2002) observed similar responses. Apparently, after a period of AA restriction, the extent of CG varies with pig type, or severity and duration of AA intake restriction.
During the re-alimentation phase pigs fed ad libitum consumed more feed than expected based on voluntary DEi according to NRC (1998) and grew faster than pigs fed restricted. Effects of feeding level on growth performance during the first part of the re-alimentation phase could be attributed partly to changes in gut fill and growth of visceral organs. These results are similar to observations by Bikker et al. (1996).
Wyllie et al. (1969) and De Greef et al. (1992) reported that ad libitum feed intake of growing pigs was reduced during the re-alimentation phase after restrictions in AA intake. In contrast, in this experiment ad libitum feed intake during the re-alimentation phase was not affected by previous nutrition. Differences among studies might be attributed to the duration and severity of protein intake restrictions during the growing phase. In the work of De Greef et al. (1992), AA restriction intake was severe (50% of estimated AA requirement) and prolonged (from 28 to 65 kg of BW). In agreement with the current experiment, Whang et al. (2003), who applied severe AA intake restrictions (50% of the estimated AA requirement) but for a shorter period (between 20 and 30 kg of BW), reported no effects on ad libitum feed intake during the re-alimentation phase.
Chemical and Physical Body Composition and the Distribution of Body Protein over Main Body Pools
Ad libitum fed pigs, regardless of diet AA levels during the restriction phase, attained the same body fatness (LB/PB) at the end of the re-alimentation phase (Table 4). It appears that ad libitum fed pigs had an inherent target body composition. This observation seems consistent with the theory proposed by Kyriazakis and Emmans (1992). In previous papers, Kyriazakis and Emmans (1991) and Kyriazakis et al. (1991) provided evidence that pigs which are fatter than normal, induced by feeding AA limiting diets, will attempt to correct this deviation once the limiting condition has been removed by altering the composition of growth (Ld/ Pd). In contrast, in the current experiment restricted fed pigs that were previously fed the AA-limiting diet remained fatter throughout the re-alimentation period as compared with pigs previously fed an AA adequate diet. This indicates that feeding level affects the pigs’ ability to achieve a target body composition.
Rao and McCracken (1992), Quiniou et al. (1995), Bikker et al. (1996), Coudenys (1998), and Weis et al. (2004) observed an inverse relationship between energy intake level and the PB content in the empty BW and a positive relationship between energy intake and the proportion of PB that is presented in viscera. In this experiment, similar results were observed at d 34 of the re-alimentation phase. This observation indicates that a reduction in energy intake level will increase body leanness and the fraction of the whole body protein recovered in the carcass. This feeding level effect on PB and viscera is consistent with the observed effect of feeding level observed at d 14 of the re-alimentation phase on sizes of individual organs such as liver, kidneys, and small intestine. The interactive effects of feeding level and previous AA intake level on sizes of kidney and spleen are difficult to explain and may be attributed to the small sample size.
Body Protein Deposition, Body Lipid Deposition, and Nitrogen Balance
Based on the serial slaughter data, in both ad libitum and restricted fed pigs, AA intake level during the restriction phase did not influence Pd and Ld during the re-alimentation phase. This indicates that no CPd occurred which is consistent with the growth performance data (Figure 1). The latter reflects the close relationship between ADG and Pd (NRC, 1998). Ferguson and Theeruth (2002) reported similar results. In addition, increased feed intake during the re-alimentation phase did not increase Pd, but increased Ld. This observation is consistent with Campbell et al. (1983) and Campbell and Taverner (1988). In ad libitum fed pigs, observed Ld and Pd from serial slaughter data are not consistent with the BW effects on body composition (Table 4). Body composition data suggest that the ratio of Ld to Pd is greater in pigs ad libitum fed AA+ than pigs on AA–. However, the SE associated with the Ld derived from serial slaughter data are rather high. This discrepancy might be eliminated if a larger number of animals were evaluated.
The numerically greater Ld in ad libitum fed pigs on AA+ did not coincide with changes in feed intake. This might indicate that pigs on AA– were energetically less efficient than pigs on AA+ during the entire re-alimentation phase. Retained energy was, at similar levels of energy intake, 8,027 and 8,854 kJ/d for pigs on AA– and AA+, respectively.
Based on N balance, pigs fed ad libitum had greater Pd than restricted fed pigs only during the first 6 d of the re-alimentation phase. This effect is attributed to the increase in Pd in visceral organs. The numerically greater Pd observed during the third and fourth period of N-balance in pigs on AA– than pigs on AA+ is consistent with observed ADG during the second part of the re-alimentation phase. However, over the entire re-alimentation phase Pd and ADG were very similar for pigs on AA– and AA+.
The results of serial slaughter and N-balance observations are not entirely consistent. Commonly, Pd calculated from serial slaughter data are lesser than N-balance derived values. This difference can be attributed to incomplete collection of N excretion and body N losses when measuring N-balances (e.g., Möhn and de Lange, 1998).
Based on serial slaughter Pd was not affected by feed intake level during the re-alimentation phase; whereas, N balance showed a response to feeding levels during the first 6 d. These results might indicate that the N-balance technique is more sensitive to short time changes in Pd than serial slaughter measurements. The serial slaughter assay yielded essentially only 1 static estimate of Pd that applied to the entire re-alimentation phase.
The literature indicates that pigs have a genetically determined PdMax (Tullis et al., 1986; Möhn and de Lange, 1998; Emmans and Kyriazakis, 1999; De Lange et al., 2001). Previous studies in our laboratory (Möhn and de Lange, 1998) showed that PdMax, in gilts from this population of pigs, was 152 g/d and remained constant between 25 to 70 kg of BW. In the current study, Pd during the re-alimentation phase was not influenced by AA intake during the restriction phase and feed intake level. Based on the serial slaughter data and during the re-alimentation phase, barrows that were previously fed AA adequate or deficient diets reached rates of Pd of 156 and 157 g/d, respectively (Figure 2). Moreover, an increase in energy intake during the re-alimentation phase increased Ld, whereas Pd remained unchanged. Observed rates of Pd during the re-alimentation phase are thus consistent with values for PdMax observed by Möhn and de Lange (1998).
As reported by Kyriazakis et al. (1991), De Greef et al. (1992), and Whang et al. (2003), pigs that were previously fed diets limiting in protein increased Pd and reduced Ld during the re-alimentation phase to reduce body fatness. In contrast, Ferguson and Theeruth (2002) showed no CPd after a period of AA intake restriction. In the current experiment and during the re-alimentation phase, restricted-fed pigs that were previously fed an AA–deficient diet grew apparently at their maximum capacity for Pd and were unable to adjust Ld to reduce LB. Therefore, nutrition induced differences in body composition during the restriction phase were maintained throughout the re-alimentation phase. However, pigs fed ad libitum achieved the same body composition at the end of the realimentation phase by altering Ld and not Pd. This apparent discrepancy between restricted and ad libitum fed pigs could not be attributed to feed intake levels and deserves further exploring.
Calculated lysine utilization was much poorer than maximal lysine utilization efficiencies observed in other N balance experiments conducted under similar conditions (Möhn et al., 2000). This indicates that intake of lysine and balanced protein during the re-alimentation period did not limit Pd and that observed Pd was determined by either energy intake or PdMax.
In conclusion, based on the current findings and a limited number of pigs per treatments, no CG and CPd occurred in pure-bred Yorkshire barrows with medium lean tissue growth potentials after AA intake restriction between 15 and 35 kg of BW. The results of this experiment suggest that PdMax is the main factor that limited the expression of CPd in this population of pigs. The current study also shows that pigs have an inherent target chemical body composition (LB/PB) and that ad libitum fed pigs may reduce Ld, rather than increasing Pd, to achieve that target LB/PB after a period of AA restriction. The concepts of PdMax and target LB/ PB may be used to explain why CG and CPd are observed in some studies and not in others.
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Footnotes |
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2 Corresponding author: cdelange{at}uoguelph.ca
Received for publication April 24, 2007. Accepted for publication April 16, 2008.
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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