Canadian Poultry Magazine

Oxygen Supplementation

By U. Sahan A. Ipek O. Altan B. Yilmaz-Dikmen   

Features Profiles Researchers

Researchers study its effects during the last stage of incubation on broiler performance and ascites

Broiler chickens are intensively selected for productive traits.
Extreme selection pressure towards either growth rate or feed
conversion ratio puts high demands on the metabolic processes in
broilers.

oxy1  
More oxygen, please. Oxygen supplementation in the incubator can be an effective means of improving hatchability.


 

Broiler chickens are intensively selected for productive traits. Extreme selection pressure towards either growth rate or feed conversion ratio puts high demands on the metabolic processes in broilers1. This has resulted in anatomical and physiological limitation of blood flow through their lungs, with deficient oxygenation of their tissues as a consequence2.

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Oxygen requirement is the most critical trigger of ascites in broilers3. Ascites susceptibility is particularly pronounced during the period of rapid juvenile growth when the metabolic rate is very high1. Although the peak incidence of ascites occurs in the fifth or sixth week of the growing period, the etiology of the disease may be initiated much earlier, even during the embryonic stage4).

Rapid growth increases the oxygen requirement, cardiac output, and blood flow and may result in increased pulmonary arterial pressure primarily by increasing the metabolic demand for oxygen5. Chicken embryos grow rapidly over the last seven days of incubation, resulting in a 60 per cent increase in the oxygen consumption during the interval between the start of breathing and hatching6.

Researchers have suggested that oxygen supplementation from 18 to 21 days of incubation could be used as an effective means of improving hatchability of broiler eggs.7 Right ventricular failure and ascites are responses to the increased workload by the right ventricle as a result of pulmonary hypertrophy. Right ventricle to total ventricle (RV:TV) ratio can be used to determine the ascites status of a bird before gross lesions are apparant.8

The aim of the current study was to determine the effect of using supplemental oxygen treatment during the last three days of incubation on broiler performance and ascites susceptibility.

Methodology
A total of 720 eggs were obtained on the same day from a commercial broiler breeder flock (Ross 308) at 40 weeks of age. The eggs were sanitized and stored at 18 C and 75 per cent relative humidity (RH) for five days. The eggs were incubated in an incubator (Cimuka A1, Ankara, Turkey) at 37.2 C and 54 per cent RH for 18 days. On the 18th day of incubation, all eggs were candled and 650 fertile eggs were randomly divided into two groups. The first group was placed in a hatcher cabinet at normal atmospheric condition. The second group was placed in a hatcher cabinet that was supplemented with oxygen from 18 to 21 days of incubation. The partial pressure of oxygen within this cabinet was regulated with a flow rate of approximately five litres per minute. The percentage oxygen was monitored daily with the use of an oxygen analyzer. Both cabinets were maintained at 36.5 C and 72 per cent RH. Digital thermometers were used in each hatcher cabinet to verify set point temperatures. After hatching, 270 chicks per treatment (normal atmospheric condition and supplemental O2 at hatching) were reared. The chicks were weighed and coded. They were randomly distributed into 12 pens (six replicates of 45 chicks per pen, for each group). The chicks were brooded at 32.5, 29 and 27 C during Weeks 1, 2, and 3 respectively. From the third week, all broilers were reared at a constant temperature of 21 C.

The feed in pellet form was formulated according to the specifications of the NRC (1994)9. Feed and water were provided ad libitum. The lighting schedule was 24 hours of light from Days 1 to 5 and 23 hours of light per one hour dark thereafter. Individual body weights were recorded at one, three, five and six weeks of age. Live weight gains and feed conversion ratios were calculated. Mortality and mortality due to ascites values in each pen were recorded daily. All dead birds were examined for the presence of typical ascites lesions, as determined in previous publications, and mortalities due to ascites were recorded.10 On the fifth week of the experiment, 10 chickens randomly chosen from each group were killed and the hearts were removed and dissected to obtain heart weights in order to calculate the RV:TV ratio8.

The research used a randomized-plots experimental design. The SAS (SAS, 1989) package program was used in the evaluation of statistical analysis. Differences between means were compared using the Duncan multiple range test and Chi-Square analysis was used in analysis of mortality ratios.

Results
Oxygen supplementation caused a significant increase in initial chick weight (P<0.01). The effects of oxygen supplementation on body weight (BW), growth rate and feed consumption were found to be significant at six weeks of age. Although oxygen supplementation did not have a significant effect on mortality, it is interesting to note that there was a difference of 2.59 per cent in mortalities due to ascites between the two treatment groups. It must be noted that, numerically, this was only a difference of seven birds (8-1), and thus statistically insignificant. At five weeks of age, there were no differences in right ventricle weight and the RV:TV ratio between the two groups.

Discussion
In the study, oxygen supplementation in the hatcher cabinet resulted in a heavier mean chick weight. The results are in agreement with those of Stock and Metcalfe (1984)11 and Christensen et al. (2004)12, who stated that oxygen limits the growth of the chick embryo.Liu et al. (1995) concluded that BW at eight weeks of age was correlated with embryonic O2 consumption on Days 14-19 of incubation.6 Jones (1995) reported an improvement in feed conversion ratio and an increase in BW of eight per cent when oxygen content within the hatching cabinet was maintained at 23 per cent.13 In this study, the oxygen-supplemented group had a significantly higher mean final BW, feed consumption and feed conversion ratio than the control group. The high metabolic demands of today’s fast growing broiler, together with insufficient oxygen availability, leads to hypoxia, which triggers ascites. Beker et al. (1995) demonstrated an inverse relationship between oxygen consumption and ascites incidence (R2=0.96).14 Mortality due to ascites of this nature was 0.37 per cent in the oxygen-supplemented group, compared with 2.96 per cent in the control group.

In the present study, mortality results were in agreement with those of Beker et al. (2003).15  It was concluded that oxygen supplementation from the 18th to 21st day of incubation increased chick weight, final body weight, growth rate and feed efficiency of the broilers.

1Department of Animal Science, Faculty of Agriculture, University of Uludag, Gorukle, Bursa, Turkey, 16059. 2Department of Animal Science, Faculty of Agriculture, University of Ege, Bornova, Izmir, Turkey. 3Department of Animal Husbandry and Health, Uludag University, Keles Vocational School, Keles, Bursa, Turkey, 16740

References
1.Decuypere, E., Buyse, J. and Buys, N. (2000). World’s Poultry Science, 56(4): 367-377.
2. Julian, R.J. (1993). Avian Pathology, 22: 419-454.
3. Julian, R.J. (2000). Avian Pathology, 6: 519 -527.
4. Coleman, M.A., Coleman, G.E. (1991). Misset World Poultry, 7: 33-35.
5. Wideman, R.F., Tackett, C. (2000). Poultry Science, 79: 257-264.
6. Liu, Z., McBride, B.W, Lirette, A. and Chambers, J.R. (1995). Canadian Journal of Animal Science, 75 (1): 115-119. NRC (1994)
7. Altan, O., Sahan, U., Ipek, A. and Aydn, C. (2006). Arch iv Fur Geflugelkunde, 70(2): 64-68.
8. Huchzermeyer, F.W., Deruyck, A.M.C. and Van Ark, H. (1988). Onderstepoort Journal of Veterinary Research, 55: 5-9.
9. Nutrient requirements of poultry. 9th ed. National academy of sciences.
10. Julian, R.J., McMillan, I. and Aquinton, M. (1989). Avian Pathology, 18: 675 -684. Jones, G.P.D. (1995). British Poultry Science, 36: 123-133.
11. Stock, M.K., Metcalfe, J. (1984). Respiration Physiology, 58: 352-358.
12. Christensen, V.L., Wineland, M.J., Yoldorom, I., Ort , D. T. and Mann, K.M. (2004). Journal of Animal and Veterinary Advances, 3(2): 52-65.
13. Visschedijk , A.H.J. (1968). British Poultry Science, 9: 173-184.
14. Beker, A., Vanhooser, S.L. and Teeter, R.G. (1995). Avian Diseases, 39: 285-291.
15. Beker, A., Vanhooser, S.L., Swartzlander, J.H. and Teeter R.G. (2003). Poultry Science, 82: 15501553.


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