Effects of Early Feed Restriction on Performance and Ascites Development in Broiler Chickens Subsequently Raised at Low Ambient Temperature

2006 Poultry Science Association, Inc.

Effects of Early Feed Restriction on Performance and Ascites Development in Broiler Chickens Subsequently Raised at Low Ambient Temperature ¨ zkan,*,1 I. Plavnik,† and S. Yahav† S. O *Ege University, Faculty of Agriculture, Department of Animal Science, ˙Izmir 35100, Turkey; and †ARO The Volcani Center, Institute of Animal Science, PO Box 6, Bet Dagan 50250, Israel

Primary Audience: Researchers, Broiler Managers, Extension Personnel SUMMARY The objective of this study was to examine the effectiveness of early-age growth limitation, achieved through feed restriction (FR), as a means of reducing ascites mortality in broiler chickens exposed to low ambient temperatures. Feed restriction was applied to broilers from 5 to 11 d of age so as to reduce their weight gain to about 40% of that of control broilers that were fed ad libitum (AL). At the age of 21 d the chickens were exposed to a temperature of 15°C, which induced ascites. By 46 d of age, ascites incidence and mortality in the feed-restricted birds were reduced to 15.79 vs. 36.84% and 7.89 vs. 26.32%, respectively, compared with those in the controls (P < 0.05). After feed restriction was stopped, the FR chickens had accelerated weight gain and improved feed conversion ratio from 11 to 18 d of age (P < 0.05), and by 46 d they had achieved the same body weight as the AL birds. Ascitic broilers had smaller relative breast muscle and spleen weights than those of the healthy broilers at 46 d (P < 0.05). However, the relative weights of lung, heart, and liver and the right ventricle weight per total ventricle weight (RV:TV) ratios were greater in ascitic broilers (P < 0.05). At age 37 d, when ascites had developed but not yet caused mortality, the ascitic broilers had lower plasma concentrations of the thyroid hormones thyroxine and triiodothyronine, and higher hematocrit values (P < 0.05) in comparison with the healthy ones. Ascitic birds also had lower oxygen consumption at 6 wk (P < 0.05), which agrees with information that the terminal stage of the ascites syndrome can be characterized by low oxygen consumption. We concluded that the early-age feed restriction reduced ascites incidence and mortality and prevented reduction of the thyroid hormone concentrations in male broilers reared at low ambient temperature from the age of 3 wk onward. Key words: ascites, early feed restriction, thyroid hormone, oxygen consumption 2006 J. Appl. Poult. Res. 15:9–19

DESCRIPTION OF PROBLEM Ascites in broilers is associated with factors such as fast growth rate and environmental parameters, including low ambient temperatures 1

Corresponding author: [email protected]

(Ta) and high altitude [1]. The syndrome is defined as a circuit of events between the cardiovascular and pulmonary systems responsible for metabolic demands [2]. The association of ascites with cardiopulmonary capacity and its ge-

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10 netic background have been clearly demonstrated [3, 4], and Decuypere et al. [5] concluded that the hypothyroid state associated with the decreased metabolism for maintenance that is caused by continuous selection for fast growth and improved feed efficiency might be involved in ascites. The high metabolic rate in fast-growing chickens, which increases dramatically in response to environmental conditions, leads to the development of the ascites syndrome, which may be characterized by enhancement of the erythropoiesis process [6]. This enhancement leads to a dramatic increase in the number of immature erythrocytes in the circulation and to a decline in the heart rate during early periods of growth [7]. These events lead to the development of hypoxemia [1], which can be confronted effectively by reducing oxygen demands, a measure that can be achieved by early-age feed restriction. Early growth restriction induced by feed restriction has resulted in improved feed efficiency, because of the decrease in energy requirements for maintenance, and improved carcass quality resulted from the decline in fat deposition [8, 9]. Despite this, conflicting findings have resulted from variations in the duration and severity of the restriction, but, nevertheless, restriction of feed either as nutritional quality or quantity of feed or time accessing to feeders is one of the primary management tools currently used to reduce the incidence of ascites in broiler production [1, 10, 11, 12, 13, 14, 15, 16]. Feed restriction mainly reduces growth rate and, consequently, metabolic demands, during the critical periods of the life span of a bird [11, 12, 13, 14, 15, 16, 17, 18], and it is associated with improvement in arterial oxygenation [10]. However, feed restriction can exert negative effects on the body weight at marketing age [13] and on the relative weight of breast muscle [12]. There have also been reports of negative effects on thyroid gland activity [19] and on the plasma triiodothyronine (T3) concentration [20]. Alteration in thyroid hormone metabolism in ascites-susceptible broilers has been cited by several authors [21, 22, 23, 24], and low plasma triiodothyronine (T4) concentration at low Ta has been reported to indicate thyroid insufficiency associated with ascites incidences in lines with a fast growth rate and low feed conversion ratio

(FCR) [23]. Recently, Luger et al. [24] reported that chickens that developed ascites could not produce T4 at a sufficient rate to compensate for the reduction caused by exposure to cold, which coincided with reduced T3 concentrations. A possible role of thyroid hormones in the development of the ascites syndrome has been suggested [6]. The objective of the present study was to elucidate the role of early-age food restriction on the development of the ascites syndrome and performance related parameters in broilers reared under cold conditions from 3 wk of age onward.

MATERIALS AND METHODS Experimental Design Male broiler chicks (Cobb) were obtained from a commercial hatchery and housed in battery brooders under standard management conditions for the first 5 d of age. At 5 d, 76 chicks were weighed, wing-banded, and randomly divided between 2 feeding groups with 7 replicates of 5 to 6 birds each. The chicks were exposed to Ta of 26.0 ± 1.0, 20.0 ± 1.0, and 15.0 ± 1.0°C at 7, 18, and 21 d of ages, respectively, to induce the development of ascites syndrome. At the age of 21 d, the birds were transferred to colony cages in a temperature-controlled room and kept at 15°C and 60% relative humidity until 46 d of age. Feeding Control birds were fed ad libitum (AL) during the experiment. In the growth-restricted group, chicks were exposed to feed restriction (FR) from 5 to 11 d of age; each chick was allowed a daily intake 18.7 g of feed that contained sufficient energy to support 50% of the normal growth rate. The energy allowance during FR was calculated according to the following equation modified from Plavnik and Hurwitz [9, 25]: EA = M × BW0.667 + G × GA where EA = energy allowance (kcal), M = maintenance requirement (1.5 kcal/g), BW0.667 = metabolic body weight at the beginning of the feed restriction period (5 d), G = energy requirement

¨ ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT O for 1 g of growth (2 kcal/g), and GA = growth allowance (15 g/d). A crumble form of starter diet was supplied from d 0 to 21, and a pelleted grower diet was supplied from d 21 to 46 of the experiment. The diets were designed according to the National Research Council’s recommendations [26] and contained 3,100 and 3,200 kcal/kg of metabolic energy, respectively, and 22.6 and 19.6% of crude protein, respectively. Water was available AL, and continuous fluorescent illumination was applied to the broilers during the experimental period. Individual body weights were measured at 5, 11, 18, 25, and 46 d of age. Feed consumption was recorded weekly, and FCR were determined for each replicate (cage) based on feed consumption and body weight gain including birds that died during the entire period. Blood samples were taken on d 30 and 37 from the brachial vein. The blood samples were stored at 4°C for hematocrit analyses, and an aliquot was centrifuged at 3,000 rpm for 10 min to obtain plasma, which was stored at −20°C pending further analyses. Ascites Diagnosis During the experiment, all dead chickens were diagnosed for ascites according to abdominal and pericardial fluid accumulation and right heart enlargement. At the end of the experiments, all chickens were euthanized to detect ascites according to fluid accumulation in the body cavities and to right heart enlargement [right ventricle weight per total ventricle weight (RV:TV) ratio > 0.28]. The birds that showed these symptoms were considered ascitic and were included in the analysis of all parameters regarding ascites. Birds not showing any of these symptoms were classified as healthy in all statistic analysis of each age. Birds having a slight hydropericardium but not showing right heart enlargement were also classified as healthy. Breast muscle (pectoralis major and minor), abdominal fat pad, lung, heart, liver, and spleen were dissected and weighed. The RV:TV ratios were calculated. Hematocrit Blood in heparinized microcapillary tubes was centrifuged for 7 min for hematocrit (HCT) measurements.

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Thyroid Hormones Plasma samples were radioimmunoassayed for total T4 and T3 with commercial kits [27] validated for domestic fowl [28]. The T3 assay was characterized by intraassay and interassay CV of 7.0 and 9.4%, respectively, and the T4 assay by intraassay and interassay CV of 5.0 and 7.5%, respectively. The T3 assay was carried out according to the manufacturer’s instructions without modifications, whereas in the T4 analysis 100-␮L samples were used. Oxygen Consumption On 3 consecutive days during the sixth week of age the oxygen consumption of 14 (7 from each feeding group) broilers was measured with an oxygen analyzer [29] according to the procedures of Yahav and Buffenstein [30]. Birds were chosen for measurement according to their previously measured HCT levels. For this purpose, 3 or 4 birds with high (>41%) or low (<41%) HCT were chosen from each feeding group, but the final descriptions of the birds as either ascitic or healthy were confirmed by necropsy at slaughter or death. Statistical Analysis Data, except for feed consumption and FCR, were subjected weekly to 2-way ANOVA with respect to the following main effects: ascites (ascitic or healthy birds), feeding (FR or AL feeding), and their interaction using the JMP statistics software package [31]. Body weight on d 5 was included in the model as a covariance parameter for the body weight and weight gain data. Only feeding effect was included in the statistical model for feed consumption and FCR data. Least square means were separated with Student’s t-test [32]. The distribution of ascites incidence and mortality within feeding groups were analyzed with the chi-squared test. Shapiro Wilk’s normality test was performed on all data and, if necessary, a common log transformation was applied to the T3, T4, and HCT data to obtain a normal distribution [32]. Actual values, however, are presented in the tables.

RESULTS Ascites Incidence and Mortality The feed restriction treatment reduced the total mortality, mortality from ascites, and over-

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Table 1. Distribution of total mortality, mortality from ascites, ascites defined at slaughter, and total ascites incidence within feeding groups Total mortality (%)

Mortality from ascites (%)

Ascites defined at slaughter (%)

Total ascites incidence (%)

Feed restriction (FR)

18.42 n = 7/38

7.89 n = 3/38

7.89 n = 3/38

15.79 n = 6/38

Ad libitum (AL)

39.47 n = 15/38

26.32 n = 10/38

10.53 n = 4/38

36.84 n = 14/38

28.94 n = 22/76 χ2 = 4.166*

17.10 n = 13/76 χ2 = 4.756*

9.21 n = 7/76 χ2 = 0.158

26.32 n = 20/76 χ2 = 4.438*

Trait

Overall (FR + AL)

*P < 0.05.

all ascites incidence (Table 1) significantly (P < 0.05). Ascites mortality was first observed 1 wk after cold exposure, and all mortality occurred during the fifth (6 birds) and sixth (7 birds) weeks (data not shown). Body Weight and Gain Feed restriction resulted in a lower body weight (P < 0.05; Table 2). However, at the end of the experiment, FR broilers achieved body weights similar to those of the AL birds. During the feed restriction period (d 5 to 11), the FR group gained 38.94% of the weight that the AL gained. During the first week posttreatment (d 11 to 18) the FR broilers gained significantly more weight than the AL ones (P < 0.05), which suggests that their growth accelerated during this stage of life. On the other hand, the FR birds did not show any further compensatory growth even during the later stages of life. There was no interaction between ascites and feeding regimen for body weight and weight gain at any age (Table 2). The body weights of ascitic and healthy birds differed significantly only at the age of 46 d (P < 0.05). Feed Consumption and FCR The cumulative feed consumption and FCR (5 to 46 d) did not differ between the feeding regimens (Table 3). The FR group performed better than the AL group from d 11 to 25 (P < 0.05). Relative Weights of Organs Ascites affected all carcass parameters with the exception of the abdominal fat (Table 4).

At slaughter age, ascitic broilers had smaller relative weights of breast muscle and spleen than those of the healthy birds, but the relative weights of lung, heart, and liver and RV:TV ratios were greater in the ascitic ones (P < 0.05). The feeding regimen did not affect any of these above parameters (Table 4). No interactions among the treatments were observed in their effects on any of these traits. Hematocrit A significant effect of ascites on HCT was observed at 37 d of age (P < 0.05; Table 5). Ascitic birds had significantly higher hematocrit values than the healthy birds. However, the feeding regimen did not affect the HCT measurements at 30 and 37 d. T3 and T4 Hormones The plasma T3 concentration was significantly lower in ascitic than in healthy broilers at 30 and 37 d of age (P < 0.05) but was not affected by FR at these ages (Table 5). The plasma T4 concentration was lower in ascitic than in healthy birds only at 37 d of age, whereas FR birds exhibited a significantly higher plasma T4 concentrations than the AL birds at 30 d (P < 0.05; Table 5). The interaction of ascites × feeding regimen was not significant for either trait at any age. However, at 30 d of age in the FR group, T3 levels of ascitic broilers were similar to those of healthy birds (2.51 and 2.62 ng/mL, respectively), whereas in the AL group T3 levels differed significantly (P < 0.05) between ascitic and healthy broilers (1.92 and 2.99 ng/mL, respectively; data not shown).

0.887 0.989 0.672 —

100 ± 2.6 (n = 38) 100 ± 2.0 (n = 38)

101 ± 2.8 (n = 20) 100 ± 1.6 (n = 56)

d5

0.961 <0.001 0.460 <0.001

174 ± 3.3b (n = 38) 290 ± 2.5a (n = 38)

232 ± 3.6 (n = 20) 232 ± 2.1 (n = 56)

d 11

12.8b 38) 9.6a 38)

13.9 20) 7.8 56)

0.973 0.001 0.929 0.001

507 ± (n = 569 ± (n =

538 ± (n = 538 ± (n =

d 18

0.145 0.026 0.326 0.136

921 ± 29.9b (n = 37) 1,006 ± 22.7a (n = 37)

936 ± 32.7 (n = 20) 991 ± 18.4 (n = 54)

d 25

± 93.7 = 31) ± 85.9 = 23)

0.047 0.565 0.281 0.001

P-values

2,726 (n 2,800 (n

2,633 ± 117.7b (n = 7) 2,892 ± 47.4a (n = 47)

d 46

0.961 <0.001 0.459 <0.001

74 ± 3.3b (n = 38) 190 ± 2.5a (n = 38)

132 ± 3.6 (n = 20) 132 ± 2.0 (n = 56)

d 5–11

± = ± =

± = ± = 12.3a 38) 9.0b 38)

13.5 20) 7.5 56)

0.977 0.001 0.919 0.585

332 (n 279 (n

305 (n 306 (n

d 11–18

± 29.2 = 37) ± 22.2 = 37)

± 31.9 = 20) ± 18.0 = 54)

0.146 0.392 0.345 0.846

747 (n 716 (n

704 (n 758 (n

d 11–25

Body weight gain (g)

0.060 0.904 0.208 0.001

1,769 ± 92.5 (n = 31) 1,753 ± 84.8 (n = 23)

1,640 ± 116.1 (n = 7) 1,881 ± 46.8 (n = 47)

d 25–46

1

a,b

Values with different superscripts for each main effect within age (column) differ (P < 0.05). Classification of the birds as ascitic or healthy. Ascites data were derived from dead birds plus those inspected at the end of the experiment and having fluid accumulation in the abdomen, pericardium, or both and right heart enlargement (right ventricle weight per total ventricle weight > 0.28).

Source of variation Ascites Feeding Ascites × feeding BW at 5 wk

Ad libitum

Feeding Feed restriction

Healthy

Ascites Ascitic

1

Body weight (g)

Table 2. Effect of ascites and feeding regimen on body weight and weight gain of boilers at different ages

¨ ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT O 13

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FCR

1.95 ± 0.06 1.88 ± 0.06

0.434

Feed consumption

5,179 ± 86.92 5,337 ± 86.92

0.223

DISCUSSION

FCR

2.08 ± 0.08 1.93 ± 0.08

0.206

The results obtained emphasize the significant and positive effects of feed restriction in preventing the development of the ascites syndrome in broiler chickens.

Oxygen Consumption Oxygen consumption was lower in ascitic than in healthy birds (P < 0.05; Table 6). Feeding did not affect oxygen consumption and the ascites × feeding interaction was not significant.

0.495 0.003 Values with different superscripts for each treatment within columns differ (P < 0.05). FR = feed restriction; AL = ad libitum. 1

0.001

0.051

0.001

0.010

P-values <0.001

112 ± 8.03b 233 ± 8.0a Feeding FR AL

a,b

508 ± 12.29b 545 ± 12.29a 1.51 ± 0.04a 1.22 ± 0.04b

Feed consumption FCR Feed consumption 1

Source of variation Feeding

1.52 ± 0.05b 1.96 ± 0.05a

Feed consumption

1,290 ± 27.89b 1,408 ± 27.89a

FCR

1.67 ± 0.05b 1.95 ± 0.05a

Feed consumption

3,777 ± 81.68 3,695 ± 81.68

Performance and Mortality

FCR

d 11–25 d 11–18 d 5–11

Table 3. Feed consumption (g) and feed conversion ratios (FCR; g/g) of feeding groups at different ages

d 25–46

d 5–46

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Feed restriction from 5 to 11 d of age reduced weight gain (to 38.9% of that in the AL broilers) and reduced FCR during the restriction period. Following the restriction period (11 to 18 d of age), compensatory growth was observed in the FR birds. It seems that the severity of the restriction period allowed full growth compensation up to the marketing age, as was previously reported [8, 9, 11, 17, 20, 22, 33, 34, 35]. The FR resulted in a marked reduction of ascites incidence and mortality compared with AL feeding, which is consistent with previous findings [11, 18, 13, 14]. In general, susceptibility to ascites has been associated with high growth rates [1, 36], and a positive correlation between potential growth rate and percentage ascites has been reported by Deeb et al. [37]. In the present study, the retardation of growth rate during the FR period could have been the main reason for the decline in ascites incidences and mortality, but it should be noted that other studies have found that ascitic broilers are not necessarily the fastest growing individuals in the flock [4, 24, 38, 39]. Furthermore, detrimental effects of ascites on body weight have been reported previously [1, 38], and those findings are consistent with the lower body weights of ascitic broilers at marketing age that was found in the present study. Acceleration of growth in FR broiler accompanied with low ambient temperature could result in hypoxemia and trigger the ascites. However, this was not the case and FR resulted in late maturity and lower incidence of ascites in this experiment, which that FR might affect the development of ascites in a critical stage prior to low Ta exposure. In general, the present findings on the relative weights of carcass parts and internal organs and

n = 31 n = 20

Feeding2 FR AL

0.023 0.953 0.145

15.39 ± 0.59 15.34 ± 0.54

14.43 ± 0.74b 16.31 ± 0.30a

0.131 0.457 0.741

1.10 ± 0.13 1.25 ± 0.14

1.03 ± 0.18 1.32 ± 0.07

Abdominal fat (%)

<0.001 0.617 0.315

0.45 ± 0.01 0.46 ± 0.01

0.50 ± 0.02a 0.41 ± 0.01b

Lung (%)

0.017 0.993 0.453

P-values

0.67 ± 0.03 0.68 ± 0.03

0.72 ± 0.04a 0.63 ± 0.01b

Heart (%)

<0.001 0.725 0.525

2.23 ± 0.08 2.19 ± 0.07

2.44 ± 0.10a 1.97 ± 0.04b

Liver (%)

0.016 0.691 0.509

0.11 ± 0.01 0.10 ± 0.01

0.08 ± 0.02b 0.13 ± 0.01a

Spleen (%)

<0.001 0.421 0.757

0.28 ± 0.02 0.32 ± 0.01

0.36 ± 0.02a 0.24 ± 0.01b

RV:TV ratio

1

a,b

Values with different superscripts for each main effect within a column differ (P < 0.05). Classification of birds as ascitic or healthy; ascitic data were derived from dead birds plus those inspected at the end of the experiment and having fluid accumulation in the abdomen, pericardium, or both and right heart enlargement (RV:TV > 0.28). 2 FR = feed restriction; AL = ad libitum.

Source of variation Ascites Feeding Ascites × feeding

n=7 n = 44

Ascites1 Ascitic Healthy

Breast muscle (%)

Table 4. Effect of ascites and feeding regimen on relative carcass parts and organs weight (%) of broilers and right ventricle per total ventricular weight (RV:TV) ratios at 46 d of age

¨ ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT O 15

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Table 5. Effect of ascites and feeding regimen on hematocrit (HCT), triiodothyronine (T3), and thyroxine (T4) levels of broilers at 30 and 37 d of age HCT (%)

T3 (ng/mL) d 30

T4 (ng/mL)

d 30

d 37

d 37

d 30

d 37

36.95 ± 1.03 (n = 18) 36.19 ± 0.59 (n = 40)

40.24 ± 1.31a (n = 13) 36.59 ± 0.67b (n = 48)

2.21 (n 2.80 (n

± 0.20b = 12) ± 0.16a = 18)

1.94 (n 2.73 (n

± 0.26b = 10) ± 0.19a = 19)

3.29 (n 3.03 (n

± 0.33 = 12) ± 0.26 = 18)

1.43 (n 2.48 (n

± 0.32b = 10) ± 0.23a = 19)

35.89 ± 0.91 (n = 32) 37.25 ± 0.76 (n = 26)

37.64 ± 1.12 (n = 33) 39.19 ± 0.96 (n = 28)

2.56 (n 2.45 (n

± 0.19 = 13) ± 0.16 = 17)

2.56 (n 2.11 (n

± 0.23 = 15) ± 0.23 = 14)

3.78 (n 2.54 (n

± 0.33a = 13) ± 0.26b = 17)

2.12 (n 1.79 (n

± 0.28 = 15) ± 0.28 = 14)

1

Ascites Ascitic Healthy Feeding FR2 AL

P-values Source of variation Ascites Feeding Ascites × feeding

0.524 0.256 0.150

0.024 0.364 0.256

0.028 0.650 0.069

0.021 0.171 0.375

0.546 0.007 0.224

0.014 0.415 0.289

Values with different superscripts for each main effect within age (column) differ (P < 0.05). Classification of birds as ascitic or healthy; ascitic data were derived from dead birds plus those inspected at the end of the experiment and having fluid accumulation in the abdomen, pericardium, or both and right heart enlargement (right ventricle weight per total ventricle weight > 0.28). 2 FR = feed restriction; AL = ad libitum. a,b 1

on the RV:TV ratios of ascitic broilers are consistent with previous results [1, 4, 5]. Increased RV:TV ratios and relative weights of heart, lung, and liver reflected the enlargement of the right side of the heart and edema in the supply organs. Table 6. The effects of ascites and feeding regimen on oxygen consumption of broilers at the age of 6 wk

Ascites1

Oxygen consumption (mL/g per h; STP)2

Ascitic Healthy

2.22 ± 0.43b 3.29 ± 0.37a

Feeding3 FR AL

3.00 ± 0.40 2.51 ± 0.40

Source of variation Ascites Feeding a,b

P-values 0.043 0.319

Values with different superscripts for each main effect within age (column) differ (P < 0.05). Classification of birds as ascitic or healthy; ascitic data were derived from dead birds plus those inspected at the end of the experiment and having fluid accumulation in the abdomen, pericardium, or both and right heart enlargement (right ventricle weight per total ventricle weight > 0.28). 2 STP = standard temperature and pressure. 3 FR = feed restriction; AL = ad libitum. 1

The significantly lower relative weight of the spleen of ascitic broilers could be attributed to the stress responses of the birds. In general, regression of lymphoid organs (e.g., the spleen) is recognized as an important response of chickens to chronic stress [40, 41]. Significant reduction in abdominal fat pad size [8, 9, 34] and greater heart weight as a percentage of body weight [14, 20] in growth-restricted birds have been reported before, but these traits were not affected by feeding in the present study. The present findings showed that better FCR in FR than in AL broilers coincided with greater weight gain between 11 and 18 d of age, but the FR birds did not perform better than the AL ones over the whole production period. This finding is contrary to those of previous studies, which reported improvements in overall feed conversion ratio as the most consistent result of early feed restriction studies [8, 9, 13, 25, 33, 35, 42]. This difference may be attributed to the pronounced effect of cold stress on FR birds. Increased heat production rate with decreased ambient temperature has been shown in broilers [43]. In the present study the FR birds were smaller by the age of 46 d, probably because they had used a higher

¨ ZKAN ET AL.: EARLY FEED RESTRICTION AND ASCITES DEVELOPMENT O proportion of energy for maintenance than for growth. HCT, Thyroid Hormones, and Oxygen Consumption Ascites had a significant effect on HCT levels at 37 d of age, and an increased HCT level is one of the defining characteristics of the ascitic broiler [15, 24, 44, 45]. The lowest levels of T3 and T4 hormones that were observed at the ages of 30 and 37 d in the present study are in accordance with the results of Luger et al. [24], who reported lower plasma T3 and T4 concentrations in ascitic broilers than in healthy birds approximately 1 wk before the death of the former. Plasma T4 concentrations in the FR broilers were higher than those in the AL birds at d 30, and increased thyroid hormone activities during the compensatory growth period was to be expected [13, 19]. The similarity of the T3 levels in the ascitic and healthy FR broilers at 30 d of age (2.51 and 2.62 ng/mL, respectively; data not shown) may lead to the conclusion that FR birds were able to keep plasma levels of T3 high until they developed ascites. This, in turn, may indicate that growth restriction resulted in enhanced recovery of thyroid gland functions. However, even if this recovery was better, it was not to a high enough level to prevent ascites development in all the FR broilers. The significantly lower oxygen consumption in the ascitic broilers was measured at the age of 6 wk, when the syndrome was already developing, as was to be expected under cold conditions that result in additional demands on the metabolic load on the birds. Increased incidence of ascites due

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to hypoxemia under cold and low oxygen pressure conditions (high altitude) have been suggested [1, 7, 15, 22, 46]. Our findings were consistent to the earlier study of Scheele at al. [47], who suggested that low oxygen consumption per metabolic body weight at low Ta indicated inadequate metabolic action and could lead to pulmonary hypertension syndrome (PHS) and, finally, ascites in broilers. It coincided with higher HCT levels in a male line selected for improved FCR and growth rate as compared with a standard broiler stock. In a recent study, Malan et al. [48] confirmed the association between ascites incidence and low heat production, thus oxygen consumption, per metabolic body weight. In the present study the reduction in oxygen consumption could have been related to the development of the syndrome, which impaired the overall performance of the broilers (i.e., feed intake and weight gain). It can be concluded that FR significantly reduced the development of ascites, as it can be induced by other methods (e.g., light restriction, dietary energy, or using mash vs. pellet diets) [11, 16, 49, 50, 51]. The FR induced better FCR in FR broilers, which consequently exhibited greater weight gain from d 11 to 18. However, the FR broilers did not retain this advantage over the AL birds for the whole of the production period, possibly because of the more pronounced effect of cold stress on the FR birds than on the AL ones in the present study. The lower oxygen consumption observed in the ascitic birds during their sixth week of age could be attributed to the overall deterioration of the birds’ conditions. However, further research is required to elucidate this question.

CONCLUSIONS AND APPLICATIONS 1. The FR significantly reduced the development of ascites and could be used effectively as a management treatment to prevent the development of the syndrome. 2. The FR used from d 5 to 11 enabled the broilers to compensate for weight gain deficiency during the treatment and to reach the same BW as the AL birds by marketing age (d 46). 3. Terminal stages of ascites syndrome could be characterized by low oxygen consumption.

REFERENCES AND NOTES 1. Julian, R. J. 1993. Ascites in poultry. Avian Pathol. 22:419– 454. 2. Currie, R. J. W. 1999. Ascites in poultry: Recent investigations. Review. Avian Pathol. 28:313–326.

3. Wideman, R. F., Jr., Y. K. Kirby, R. L. Owen, and H. French. 1997. Chronic unilateral occlusion of an extrapulmonary primary bronchus induces pulmonary hypertension syndrome (ascites) in male and female broilers. Poult. Sci. 76:400–404.

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4. Wideman, R. F. 2000. Cardio-pulmonary hemodynamics and ascites in broiler chickens. Avian Poult. Biol. Rev. 11:21–43.

temperature on partial efficiencies of protein and fat retention and plasma hormone concentrations. Br. Poult. Sci. 40:140–144.

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