HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparalpha pathway. This metabolic adaptation to oxygen conservation impairs oxidative muscle performance in healthy conditions, but it provides acute protection of myofibers against lethal ischemia. Hypoxia tolerance is not due to HIF-dependent angiogenesis, erythropoiesis or vasodilation, but rather to reduced generation of oxidative stress, which allows Phd1-deficient myofibers to preserve mitochondrial respiration. Hypoxia tolerance relies primarily on Hif-2alpha and was not observed in heterozygous Phd2-deficient or homozygous Phd3-deficient mice. Of medical importance, conditional knockdown of Phd1 also rapidly induces hypoxia tolerance. These findings delineate a new role of Phd1 in hypoxia tolerance and offer new treatment perspectives for disorders characterized by oxidative stress.

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A total of 1,800 incubating eggs produced by a commercial flock of Cobb broiler breeders was used to determine the effects of storage duration (3 or 18 d) on spread of hatch and chick quality. Chick relative growth (RG) at the end of 7 d of rearing was also determined as a measure of the chick performance. Chick quality was defined to encompass several qualitative characteristics and scored according to their importance. Eggs stored for 3 d hatched earlier than those stored for 18 d (P < 0.05). Hatching was normally distributed in both categories of eggs, and the spread of hatch was not affected by storage time (P = 0.69). Storage duration of 18 d reduced the percentage of day-old chick with high quality as well as average chick quality score (P < 0.05). RG varied with length of egg storage, quality of day-old chick, and the incubation duration (P < 0.05). Eighteen-day storage of eggs not only resulted in longer incubation duration and lower quality score but also depressed RG. Chick quality as defined in this study was correlated to RG and storage time. It was concluded that day-old chick quality may be a relatively good indicator of broiler performance. The results suggest however that in order to improve performance prediction power of chick quality, it would be better to define it as a combination of several qualitative aspects of the day-old chick and the juvenile growth to 7 d.

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The health benefits of omega-3 polyunsaturated fatty acids (n−3 PUFA) are generally recognized. Unfortunately, in most western countries, the recommended daily intake of these compounds is rarely met. Therefore, enrichment of commonly occurring foods can boost intake of these fatty acids. In this regard, eggs are an interesting target, as they form an integral part of the diet. Their n−3 PUFA profile can be modified through feed supplementation. A traditional n−3 PUFA source to be added to hens' diet is flaxseed, a plant source rich in α-linolenic acid. Alternatively, hens are often fed fish oil, which is rich in long chain n−3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). A more recent trend is feed supplementation with microalgae as a source of EPA and/or DHA. In this paper, recent scientific literature concerning n−3 PUFA enrichment in eggs is reviewed, giving an overview of advantages and disadvantages of the different approaches.

Creatine, (CREA) a central constituent in energy metabolism, is obtained from dietary animal protein or de novo synthesis from guanidinoacetic acid (GAA). Especially in all-vegetable diets, supplemental CREA or GAA may restore the CREA availability in tissues, and hence, improve performance. In this study, 768 one-d-old male Ross 308 broilers were assigned to 1 of 4 diets: negative control, all-vegetable corn-soybean-based; negative control supplemented with either 0.6 or 1.2 g of GAA per kilogram of feed; and positive control (60, 30, and 30 g/kg of fish meal in the starter, grower, and finisher diets, respectively). Each treatment was replicated in 6 pens of 32 birds each. At the end of the grower period (d 26), 2 birds per pen were euthanized for metabolic measurements. Four broilers per pen were selected at slaughter age (d 39) to determine carcass characteristics and meat quality. Compared with the negative control, GAA supplementation resulted in an improved gain:feed ratio (P < 0.05) and ADG (P < 0.05; + 2.7 and + 2.2% for GAA at 0.6 and 1.2 g/kg, respectively) throughout the entire period. Breast meat yield was higher for the GAA diets compared with that of the negative control birds (P < 0.05; 30.6 vs. 29.4%) and was comparable with that of the positive control birds (30.2%). With regard to meat quality, lower ultimate pH values, higher cooking and press fluid losses, and higher color L* values were observed for the GAA diets compared with those of the negative control diet (P < 0.05). These effects were small, however. The GAA and CREA levels in breast meat were lower and higher, respectively, in GAA-fed birds compared with those of the control birds (P < 0.01). The diets did not affect plasma metabolic traits, except that plasma insulin-like growth factor I concentrations were almost twice as high in animals fed 1.2 g/kg of GAA compared with those of all other treatments. The GAA included in all-vegetable diets improved animal performance for the whole rearing period and increased breast meat yield.

Delay in access to feed for 1-d-old chicks impairs posthatch growth. It is a standard practice that 1-d-old chicks are deprived of feed for about 48 h before they are placed on farms. During incubation, there is a spread of 24 to 48 h for late versus early hatching. As spread of hatch increases, number of chicks that are feed-deprived for a longer time before free access (IA) to feed and water increases. In this current study, we investigated the effects of time delay in feed access on chick juvenile relative growth (RG: a measure of speed of growth) up to d 7, taking into consideration the duration of egg storage and spread of hatch. Our results confirmed that delay in feed access caused weight loss during holding time and depressed growth rate after access to feed. The magnitude of the effect depended on the hatching period within the hatching window. It also depended on whether the biological age (BA) or the chronological age (CA) of the chick was considered. Immediate access to feed produced significantly different results depending on CA or BA. Both ways, the method seemed to benefit the late hatchers. This finding contrasts with the effect of delayed feeding in which early hatchers benefited more. Long duration of egg storage depressed RG not only of chicks with immediate access to feed but also in those denied access after hatch. Delay in feed access significantly aggravated the effects of long egg storage duration on RG. Triiodothyronine levels were lower in feed-deprived chicks, and the effect was greater in late hatchers. It is concluded that the beginning of delay in feed access should be determined from the time of hatch not at the end of hatch. It is suggested that the adverse effects of delay in feed access can be reduced by providing a source of energy in hatching baskets or during transportation.