Respiratory efficiency and thermoregulatory responses of L-citrulline-supplemented broiler chickens under acute and chronic stress conditions.

Introduction: Poultry birds are exposed to diverse environmental stressors, including high ambient temperatures and endotoxins, which negatively affect the birds' health and productivity. This study investigated the impacts of both stressors and the mediatory role of dietary L-citrulline (LCT) on the physiological responses of broiler chickens. Methods: A total of 384, 1-day-old broiler chicks were randomly divided into 4 groups, 8 replicates of 12 chicks, and fed two dietary treatments of basal diet (CON) or basal diet supplemented with 1% LCT. At 21 days old, broilers were subjected to acute conditions of heat stress (HT:35 ℃ vs thermoneutral (TNZ:24 ℃); experiment 1) or immune stress (2 mg/kg BW lipopolysaccharide (LPS) or saline; experiment 2) and monitored for 5hours in a respiratory chamber. In the chronic LPS challenge (experiment 3), birds at 41days old were administered 1 mg/kg BW LPS at 1, 6, and 24 hours. Results and discussion: Exposure to HT conditions elevated the body temperature, O2 consumption, CO2 expiration, and heat production (HP) of broilers (P>0.05). Broilers fed the LCT diet also exhibited increased O2 consumption, CO2 expiration, and HP relative to the CON diet (P>0.05). Contrastingly, acute LPS challenge reduced the O2 consumption, CO2 expiration and HP. The provision of dietary LCT tended to reduce the core body temperature (CBT) of HT broilers and exerted significant effects by decreasing the CBT of LPS-challenged broilers (P>0.05). LCT supplementation also diminished the respiratory quotient (RQ) of broilers exposed to either HT or LPS compared to the unchallenged LCT groups, which had elevated RQ (P>0.05). The plasma inducible nitric oxide synthase levels were reduced by the LCT diet, with a consequent decline in plasma NO concentrations in experiment 3. Examining the mRNA expression of thermosensing TRP ion channels revealed that HT upregulated hypothalamic TRPV1 expression, whereas chronic LPS downregulated skin TRPV2 and TRPA1 expressions. In addition, the co-treatment of LPS with LCT further evoked a decline in skin TRPA1 expressions (P>0.05). Conclusion: Overall, this work demonstrated the capacity of HT and LPS challenge to dysregulate whole-body metabolism and the potential of dietary LCT to exert mediatory effects, which may be crucial for the reestablishment of homeostasis.