Broiler chickens start their life inside an incubator without any exogenous feed and water access, before being sorted and transported to a grow-out facility. During incubation, important organs, such as the gastro-intestinal tract and the immune system start to develop, a process that continues for several weeks after hatching. Hence, broiler chickens undergo a number of changes during the perinatal period, including the first week of life, both physiological and environmental related. Although broiler chickens have a residual yolk that may provide nutritional support during the first week of life, the period between hatch and first (exogenous) feed intake might have an impact on subsequent growth performance. Furthermore, the physiological status of the chicken at hatch determines the nutritional requirements of the chicken for this age period. Interestingly, that same physiological status also sets boundaries with respect to feed ingredients and nutrients constraints within the diet that the chicken can digest and metabolize.
Immature development of the gastro-intestinal tract is associated with a suboptimal digestive capacity for fat. To anticipate this, young broiler chickens are fed (pre-) starter diets that are primarily based on starch and protein sources that are perceived to be easily digestible at this age. Immature development of the immune system may expose the broiler chicken to a higher risk for diseases and mortality during the first week of life. Limited knowledge is available about how physiological development during the first week of life, reflected by digestive organ and immune status, is affected by feed availability directly after hatch, and macro nutrient composition in complex pre-starter diets. Furthermore, it is not well known how nutrition during the first week of life affects long-term physiological development, growth performance, and health status.
In traditional hatcheries, the time between hatch and first feed intake is variable (up to 48 or even 72 h) due to differences in the spread of hatch, processing and transportation time. Various studies have looked at the effect of time between hatch and first feed intake on development and growth later in life, but often focused on delayed feed intake in relation to large time intervals (48 to 72 h). Newly hatched chickens were pulled from an incubator at three time intervals (475 to 481, 483 to 487, and 489 to 493 h after onset of incubation) and were provided feed and water either directly or delayed (504 h after onset of incubation). The results of this study suggested that especially early hatched chickens benefit from direct feed access compared to midterm and late hatched chickens, as they tended to have a higher body weight gain from 0 to 18 d of age. Furthermore, irrespective of the moment of first feed intake, early hatched chickens were found to be physiologically different compared to midterm and late hatched chickens by means of a higher breast meat yield at 18 d of age. A short (13 to 26 h) delay in feed access after hatching resulted in lowered body weight gain and feed intake compared to direct feed access during the first week of life. In addition, delayed feed access resulted in a lower weight to length ratio.
Broiler chickens received either direct or delayed (48 h) feed access after placement in the grow-out facility. Pre-starter treatments consisted of a control diet (with soybean oil), a diet with fish oil (5 g/kg) or a diet with a blend of medium chain fatty acids (MCFA; C10:0 and C12:0; 30 g/kg), followed by a standard starter and grower diet. Immune function was measured through innate and specific humoral immunity, represented by immunoglobulins, interferon gamma, complement activity, and agglutination titres, of which agglutination titres were determined after a challenge with sheep red blood cells at 21 d of age. Results showed that chickens with direct feed access after placement that were fed the control pre-starter diet had a higher risk for mortality than chickens with delayed feed access and fed the control pre-starter diet, with the other treatment groups in between. Although the inclusion of MCFA resulted in higher body weight gain and lowered feed efficiency during the first week of life, this effect was not maintained for the remainder of the grow-out period. For direct fed chickens, the body weight at 28 d of age was highest for the control diet and lowest for the diet with MCFA, whereas this was the opposite in delayed fed chickens. The inclusion of fish oil and MCFA had minor effects on humoral immune function. Until 25 d of age, delayed feed access resulted in lowered body weight gain and feed intake compared to direct feed access, whereas gain to feed ratio was higher.
Despite that embryonic development of broiler chickens largely depends on fat oxidation, it is generally assumed that fats and oils are not well digested and metabolized by young broiler chickens. To validate this, broiler chickens were fed increased diet densities in pelleted form from 0 to 7 d of age. Increased diet densities were obtained by formulating diets with different dietary fat levels (3.5, 7.0, 10.5, 14.0, and 17.5% dietary fat). With an increase in dietary fat level, amino acid levels, mineral levels, and the premix inclusion level were increased as well to preserve a similar ratio between energy, amino acids, minerals, and premix level in the diet.
Nitrogen metabolizability and fat digestibility were not affected by diet density, but dry matter metabolizability was decreased as a consequence of increased diet densities. Furthermore, the crop, liver, and pancreas weights (as a percentage of body weight) decreased due to increased diet densities. On the contrary, the length of the entire intestinal tract (duodenum, jejunum, ileum, and cecum) increased, coinciding with an increased duodenum weight and an increased weight to length ratio for the ileum and cecum. These results suggest that increasing diet densities with increased dietary fat levels do not have to result in lowered performance per se, as the broiler chicken appears to repartition visceral organ development in response to more concentrated diets during the first week of life.
Treatments fed different diet densities until d 7 or 14 received a 3.5% dietary fat diet for the remaining period. Regardless of feeding phase, feeding increased diet densities resulted in a higher ME intake, ADG, and gain to feed ratio during the period these diets were provided. Feeding increased diet densities until 7 d of age had no effect on overall (0 to 34 d of age) growth performance, whereas feeding increased diet densities until 14 d of age resulted in increased body weight gain and feed efficiency from 0 to 34 d of age. The relative decrease in body weight gain as a result of switching from a high to a low density diet was higher when feeding increased diet densities until 14 d of age compared to 7 d of age. Metabolizable energy efficiency was only affected from the first week of life onwards. Continued feeding of increased diet densities resulted in higher energy efficiencies, but this effect disappeared when changing to a low density diet. When the metabolizable energy efficiency was corrected for the energy requirement for maintenance, the efficiency increased when high diet density levels (12.8 and 17.5% dietary fat) were followed by a low density diet at both 7 and 14 d of age. Continued feeding of increased diet densities resulted in a higher body weight at slaughter, but a lower breast meat yield, whereas feeding increased diet densities from 0 to 14 d of age resulted in a lower fat pad weight at 34 d of age. Results suggest that feeding increasing diet densities resulted in higher BW gain, G:F ratio and metabolizable energy intake, but mainly during the periods that these diets were provided.
It can be concluded that short durations of delayed feed access impact the intestinal development of young broiler chickens. Furthermore, MCFA can be added to the diet to increase growth performance during the first week of life, especially when fed to meat chickens with delayed feed access. High density diets result in higher growth performance, but only for the period these diets are provided.